doi: 10.1161/01.RES.0000146094.59640.13
© 2004 American Heart Association, Inc.
Reviews |
Antiinflammatory Properties of HDL
From the Heart Research Institute (P.J.B., S.N., K.-A.R.), Sydney, Australia; Department of Medicine (G.M.A.), Atherosclerosis Research Unit, University of Alabama, Birmingham, Ala; and David Geffen School of Medicine, University of California at Los Angeles.
Correspondence to Philip J. Barter, The Heart Research Institute, 145 Missenden Rd, Camperdown, Sydney 2050, Australia. E-mail p.barter{at}hri.org.au
This Review is part of a thematic series on New Pathways in HDL Metabolism, which includes the following articles:
Antiinflammatory Properties of HDL
Regulation of HDL Metabolism and Reverse Cholesterol Transport In Vivo Endothelial and Antithrombotic Effects of HDL Genetics of Variation in HDL Cholesterol in Humans and Mice
Daniel Rader Guest Editor
 |
Abstract |
|---|
 Top Abstract IntroductionOxidationInflammationConclusionReferences |
|---|
There are several well-documented functions of high-density lipoprotein (HDL) that may explain the ability of these lipoproteins to protect against atherosclerosis. The best recognized of these is the ability of HDL to promote the efflux of cholesterol from cells. This process may minimize the accumulation of foam cells in the artery wall. However, HDL has additional properties that may also be antiatherogenic. For example, HDL is an effective antioxidants. The major proteins of HDL, apoA-I and apoA-II, as well as other proteins such as paraoxonase that cotransport with HDL in plasma, are well-known to have antioxidant properties. As a consequence, HDL has the capacity to inhibit the oxidative modification of low-density lipoprotein (LDL) in a process that reduces the atherogenicity of these lipoproteins. HDL also possesses other antiinflammatory properties. By virtue of their ability to inhibit the expression of adhesion molecules in endothelial cells, they reduce the recruitment of blood monocytes into the artery wall. These antioxidant and antiinflammatory properties of HDL may be as important as its cholesterol efflux function in terms of protecting against the development of atherosclerosis.
Key Words: antiinflammatory • antioxidant • atherosclerosis • high-density lipoprotein
|
Introduction |
|---|
|
TopAbstractIntroductionOxidationInflammationConclusionReferences |
|---|
In epidemiological studies, high plasma levels of high-density lipoproteins (HDLs) protect against the development of atherosclerosis.1,2 The precise mechanism is uncertain, although most likely it is the consequence of one or more of the reported actions of HDL.3 The best known of these relates to the ability of HDL to promote the efflux of cholesterol from cells in the artery wall.4 However, HDLs have additional functions, some of which may be unrelated to their role in plasma lipid transport. For example, they bind lipopolysaccharide,5 stimulate endothelial cell movement,6 inhibit the synthesis of platelet-activating factor by endothelial cells,7 and protect erythrocytes against the generation of procoagulant activity.8 HDLs stimulate prostacyclin synthesis by endothelial cells.9 They also bind prostacyclin and thus prolong its half-life.10 They reduce epidermal growth factor-induced DNA synthesis in vascular smooth muscle cells.11 HDLs are antithrombotic.12 They modulate endothelial function,13 probably by stimulating endothelial nitric oxide (NO) production.14 HDLs also possess antioxidant and antiinflammatory activities.3,15–21 The degree to which any or all of these nonlipid transport functions of HDL contribute to a protection against atherosclerosis is still uncertain, although evidence is mounting that at least some of them may be especially important.
This review focuses on the antioxidant and antiinflammatory properties of HDL (Figure 1). It summarizes the role of oxidation and inflammation in atherogenesis and describes how these processes may be inhibited by HDL. It concludes with an assessment of the potential clinical importance of the antioxidant and antiinflammatory properties of HDL.
|
|
Oxidation |
|---|
|
TopAbstractIntroductionOxidationInflammationConclusionReferences |
|---|
Role of Oxidation in Atherogenesis
The two main hypotheses of atherogenesis that have survived decades of research are the reverse cholesterol transport hypothesis4,22 and the oxidation hypothesis.3,19,23–26 Both hypotheses assign a central role to low-density lipoproteins (LDLs) in initiating atherogenesis and to HDL in mitigating the process.3,19 As discussed, these two hypotheses may be fundamentally linked.
The central role of LDL in atherogenesis is, in part, the consequence of LDLs entering the subendothelial space, where they bind to the complex matrix beneath the endothelium.27 As a result, the artery wall concentration of apolipoprotein B (apoB) in normal mammals is approximately double that found in plasma. In contrast, whereas normal HDLs readily enter the subendothelial space, they do not bind to the matrix. Hence, HDLs tend to return to the circulation. This explains why the artery wall concentration of apolipoprotein A-I (apoA-I), the main protein in HDL, is normally only 10% to 20% of that found in plasma.
LDLs provide the main pathway for transporting cholesterol and phospholipids into mammalian cells. Navab et al reported that normal circulating LDL always contains small quantities of lipid hydroperoxides derived from the lipoxygenase pathway.15 Based on studies using an in vitro artery wall model, it was concluded15,16 that the LDLs trapped in the subendothelial space receive additional lipid hydroperoxides produced by the lipoxygenase and myeloperoxidase pathways operating in cells within the artery wall. They hypothesized that when the level of oxidized lipids in the trapped LDL exceeds a critical threshold, the LDL phospholipids that contain arachidonic acid in the sn-2 position (the second position on the glycerol backbone) become oxidized and pro-inflammatory.15,16 Recognition of these oxidized phospholipids by a specific antibody, EO6 (an IgM autoantibody that recognizes the phosphatidylcholine head group in oxidized, but not in unoxidized, phospholipids containing arachidonic acid in the sn-2 position), has enabled them to be identified in atherosclerotic lesions in animals and humans.28
The 12/15-lipoxygenase pathway,15,16,29–33 the 5-lipoxygenase pathway,34–36 the myeloperoxidase pathway,37–43 the cycloxogenase pathways,44–46 and the NADPH oxidase pathways47,48 have all been implicated in atherogenesis. The work of Blair et al49,50 has shown that bifunctional electrophiles (
, ß–ß unsaturated aldehyde genotoxins) such as 4-oxo-2-noneal can be formed from different lipid hydroperoxides by the action of trace metal ions or by vitamin C. The possibility that 4-oxo-2-noneal acts on LDL to produce biologically active oxidized phospholipids that are recognized by EO6 may explain how the genetic manipulation of multiple pathways producing different lipid hydroperoxides can influence atherogenesis.
Antioxidant Properties of HDL
The main protein in HDL, apoA-I, is capable of removing LDL lipid hydroperoxides in vitro, after injection into mice in vivo, and after infusion into humans in vivo.15,16 It has also been reported that HDL CE-O(O)H (cholesteryl ester hydroperoxides) are rapidly and selectively removed by liver cells.51,52 Thus, one of the main antioxidant/antiinflammatory functions of HDL is mediated by a transport mechanism that binds and carries away oxidant molecules.
HDLs are major carriers of plasma lipid hydroperoxides in animal models of atherosclerosis19 and in humans.53 HDLs are also carriers of enzymes that destroy the lipid hydroperoxides that oxidize LDL phospholipids.18 These enzymes include paraoxonase-154–56 and paraoxoanse-3,57 and possibly glutathione phospholipid peroxidase.18 In addition, it has been shown that HDL phospholipid hydroperoxides are reduced to corresponding hydroxides with a concomitant oxidation of apoA-I methionine residues. This reducing activity of apoA-I is independent of paraoxonase.58 HDLs also transport enzymes such as platelet-activating factor acetyl hydrolase59 and lecithin cholesterol ester acyltransferase60 that are able to remove EO6-positive oxidized phospholipids.
It has been suggested that HDL evolved as part of the innate immune system.18 HDLs account for a significant component of the antiviral activity of human plasma.61 Van Lenten et al62 reported that HDLs lose their antiinflammatory properties during acute influenza infection. HDLs isolated from mice infected with influenza A virus lose their ability to protect LDLs against oxidation by human artery wall cells and are ineffective in preventing the LDL-induced monocyte chemotactic activity in a human artery wall coculture.62 In other studies, LDL receptor-null mice were infected with influenza A virus. They were then treated with injections of an apoA-I mimetic peptide, D-4F, or vehicle alone. Those receiving vehicle alone had an increase in macrophage trafficking into the aortic arch and innominate arteries.63 In contrast, the mice receiving injections of D-4F had no increase in macrophage trafficking into the aortic arch and innominate arteries.63 In vitro, D-4F63 was shown to be comparable to apoA-I64 in terms of its ability to inhibit macrophage cytokine production induced by T cells.
The mechanism underlying these properties of the apoA-I mimetic peptide, D-4F, was further investigated in cultures of human type II pneumocytes infected with influenza A in the presence or absence of D-4F.65 It was concluded that human type II pneumocytes respond to influenza A infection by activating caspases and by secreting cytokines and phospholipids (including oxidized phospholipids that evoke inflammatory responses) into the extracellular environment and that treatment with the apoA-I mimetic D-4F inhibits these events.
|
Inflammation |
|---|
|
TopAbstractIntroductionOxidationInflammationConclusionReferences |
|---|
Role of Inflammation in Atherogenesis
It is now well-accepted that atherosclerosis is a chronic inflammatory disorder characterized by an accumulation of macrophages and T lymphocytes in the arterial intima66,67 and an increased plasma concentration of several inflammatory markers.68–70 The macrophages accumulating in atherosclerotic plaques are derived mainly from blood monocytes that adhere to endothelial cells before migrating into the subendothelial space. Within the artery wall, the monocytes differentiate into macrophages that express a range of scavenger receptors, some of which have the ability to bind and internalize (modified) LDLs. The foam cells that result are considered to be the hallmark cells of atherosclerosis.
An early step in this inflammatory process is the adhesion of monocytes to endothelial cells that have been injured or stimulated in some other way to express adhesion proteins. Shih et al have reported that this process begins with monocyte adhesion to endothelial connecting segment-1 via activation of ß1 integrins.71 Activated endothelial cells express several adhesion proteins, including vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin.72,73 These adhesion proteins are known to be expressed in arteries in vivo at sites of developing atherosclerosis,74 and soluble forms are present at increased concentrations in the plasma of human subjects with coronary heart disease (CHD).73 Once they bind to adhesion proteins on the surface of endothelial cells, monocytes are retarded and available for recruitment into the subendothelial space by chemokines such as monocyte chemotactic protein-1 (MCP-1). The discovery that human HDLs inhibit endothelial cell adhesion molecules and MCP-120,21 is thus of potentially great importance.
Endothelial Cell Adhesion Proteins and Chemokines
E-selectin is expressed in endothelial cells in response to activation by proinflammatory cytokines via the nuclear transcription factor, nuclear factor kappa ß (NF-
B). It mediates the rolling and loose tethering of leukocytes on the luminal surface of endothelial cells before they are more tightly bound by VCAM-1 and ICAM-1, both of which are members of the immunoglobulin superfamily.75–77 ICAM-1 is constitutively expressed on endothelial cells and leukocytes, and it interacts with leukocyte-specific integrins. VCAM-1 is expressed on endothelial cells in response to inflammatory cytokines and, like ICAM-1, interacts with integrins on the surface of leukocytes. ICAM-1 and VCAM-1 promote firm adhesion and subsequent arrest of leukocytes on the surface of endothelial cells.75–77
The expression of endothelial cell adhesion proteins is increased in vitro in response to several stimuli, including activation by pro-inflammatory cytokines.72,78 In addition, animal studies have demonstrated the increased expression of endothelial cell adhesion proteins in response to cholesterol feeding,79 altered shear stress,80 and balloon injury.81 Their expression after balloon injury parallels the development of abnormal acetylcholine-induced vasodilatation.81
Studies of genetically engineered mice and of mice treated with monoclonal antibody against VCAM-1 support a role of adhesion proteins in atherogenesis.82–84 Antibody blockade of the VCAM-1 ligand, VLA-4, has been reported to reduce neointimal formation after carotid injury in primates.85 It has been proposed that the atheroprotective effects of antibodies directed against the CD40 ligand are achieved by an inhibition of endothelial cell VCAM-1 expression.86 The effects of reduced ICAM-1 expression are inconsistent, with both positive87 and negative88 results reported. Various selectins and members of the immunoglobulin superfamily also exist in a soluble plasma form in concentrations that have been shown in some studies to correlate with the presence of other cardiovascular risk factors.89,90
Monocyte chemoattractant protein-1 is produced by endothelial cells in response to abnormal shear stress, oxidized LDL, and vascular injury, such as balloon angioplasty.91 Its generation within the arterial wall produces a gradient that promotes migration into the artery wall of any leukocytes that have been retarded by binding to endothelial adhesion proteins.
Effect of HDL on Transmigration of Monocytes
In vitro studies have shown that HDLs inhibit monocyte transmigration in response to oxidized LDL.92 This property appears to be related to paraoxonase and platelet-activating factor acetyl hydrolase on HDL and is reduced in acute inflammatory states as a consequence of the HDL accumulating serum amyloid A.93 This effect of serum amyloid A is in contrast with its lack of influence on the tumor necrosis factor (TNF)-–mediated expression of endothelial cell adhesion proteins.94 The explanation for this apparent inconsistency is not known. In another study it was found that HDL isolated from patients with documented CHD (but without low plasma HDL concentrations) did not inhibit monocyte chemotaxis to the same extent as the HDL isolated from control subjects without CHD.95
Inhibition of Endothelial Cell Adhesion Proteins by HDL
Several groups have shown that HDLs inhibit the expression of cell surface adhesion molecules by activated endothelial cells in vitro.96–98 Both native HDL and reconstituted HDL (rHDL) containing only apoA-I and phosphatidylcholine96,99 inhibit the cytokine-induced expression of VCAM-1, ICAM-1, and E-selectin by human umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner within the range of physiological HDL levels. The inhibition of adhesion molecule expression is associated with a reduction in the mRNA levels of these proteins.96,99 The in vitro inhibition of cytokine-induced expression of endothelial cell VCAM-1 is time-dependent, with the magnitude of inhibition increasing with duration (up to 16 hours) of the pre-incubation. However, having undergone a period of pre-incubation, the rHDL can be removed from the cells before adding the TNF-, without any apparent loss of inhibition of the adhesion molecule expression, indicating that the inhibition is not the consequence of HDL interfering with the binding of TNF- to its receptor.100 Furthermore, once the inhibitory effect of rHDL on endothelial cells has been achieved by pre-incubation, the inhibition persists for several hours after the rHDLs have been removed.100 These findings imply that exposure to the rHDL modifies the cells in some way to make them resistant to cytokine-induced expression of VCAM-1 in a time-dependent process.
The HDL isolated from the plasma of different human subjects vary in their inhibitory activity (Figure 2);101 the reason for the variation is uncertain. It is well-known that the HDL fraction in human plasma is heterogeneous, consisting of a number of discrete subpopulations that vary in size, density, and composition of lipids and apolipoproteins. It has been reported that the inhibitory activity of the HDL3 subfraction (in which the particles are smaller and denser) is superior to that of HDL2 (in which the particles are larger and less dense),101 although this did not explain the observed variation in inhibitory activity of the HDL isolated from different subjects. Discoidal and spherical rHDL of defined size and chemical composition have been used to investigate how varying the morphology and composition impacts on the ability of HDL to inhibit the TNF-–induced expression of VCAM-1 in endothelial cells. Inhibition appears to be unaffected by variations in HDL particle size or in the composition of apolipoproteins, cholesteryl esters, or triglyceride.102 In marked contrast, varying the composition of phospholipids in HDL has major effects on their inhibitory activity.103
|
Studies were conducted with rHDL to determine the ability of different phosphatidylcholine (PC) species to inhibit cytokine-induced expression of VCAM-1 in HUVECs (Figure 2).103 PC species containing palmitoyl- in the sn-1 position and either palmitoyl- (DPPC), arachidonyl- (PAPC), linoleoyl- (PLPC), or oleoyl- (POPC) in the sn-2 position were compared. These PC species were studied as components of discoidal rHDL containing apoA-I as the sole protein or as small unilamellar vesicles. The rHDL containing PLPC and PAPC inhibited VCAM-1 expression in activated HUVECs by 95% and 70%, respectively, at an apoA-I concentration of 16 µmol/L. At this concentration of apoA-I, POPC rHDL inhibited by only 16% and DPPC rHDL did not inhibit at all. These differences could not be explained by differential binding of the rHDL to HUVECs.103
The same hierarchy of inhibitory activity was observed when these PC species were presented to the cells as small unilamellar vesicles, but only when the small unilamellar vesicles also contained an antioxidant.103 When the antioxidant was not present, PLPC became oxidized during the vesicle preparation or during the subsequent incubation and was cytotoxic to the cells. The most likely reason why PLPC is not cytotoxic when it is present in discoidal rHDL particles is that apoA-I protects the phospholipid against oxidation, thus enabling it to retain its antiinflammatory properties. The pathophysiological implications of differences in the effects of specific HDL PC species are uncertain. This effect of the PC fatty acid composition on the inhibitory activity of HDL matches that seen when activated endothelial cells are incubated with nonesterified fatty acids.104 However, the duration of pre-incubation required for nonesterified fatty acids to demonstrate this property is much greater than that required by HDL.
It should be noted that some studies have failed to demonstrate an ability of HDL to inhibit endothelial cell adhesion molecule expression. There have been negative reports of the effects of both native HDL and rHDL on cytokine-induced adhesion molecule expression by arterial and venous endothelial cells.105,106 The reason for these discordant results is unclear.
Mechanism by Which HDLs Inhibit Adhesion Molecule Expression
HDLs inhibit endothelial cell sphingosine kinase, an enzyme that catalyzes a key step in the pathway by which TNF- stimulates the expression of endothelial cell adhesion molecules (Figure 3). 99 This inhibition of sphingosine kinase has a downstream effect by inhibiting the nuclear translocation of NF-b.99 The ability of HDL to inhibit the nuclear translocation of NF-b has been confirmed by one group,98 although another report concluded that an HDL-mediated inhibition of E-selectin is independent of NK-b.107 The explanation for this discrepancy is unclear and will have to await further research.
|
Oxidized forms of HDL may activate NF-b and promote its nuclear translocation in a process that is linked to an increase in the generation of intracellular reactive oxygen species.108 A reduction in the activation of NF-b may be secondary to a reduction in oxidative stress. NF-b is activated by reactive oxygen species and maintained in an inactive state by low levels of NO.109 The ability of HDL to inhibit reactive oxygen species generation and promote the synthesis of NO, and thus to inhibit the activation of NF-b, may therefore also contribute to their inhibition of adhesion molecule expression.
Inhibition of Chemokines by HDL
HDLs inhibit the expression of MCP-1 in response to oxidized LDL54,92 in a process linked to the antioxidant components of HDL. Furthermore, the expression of apoA-I in apoE knockout mice results in a reduced plaque expression of MCP-1 after transplantation of atherosclerotic aorta.110
HDL, C-Reactive Protein, and Atherosclerosis
The plasma concentration of C-reactive protein (CRP), an acute-phase reactant, is a predictor of cardiovascular events.68,69 There is emerging evidence that CRP may itself contribute to the inflammatory process.111 In studies of vascular cells incubated in vitro, CRP has been reported to increase secretion of MCP-1,112 reduce endothelial NO synthase bioactivity,113 and induce VCAM-1, ICAM-1, and E-selectin.111,114 In a recent study by Wadham et al, it was shown that HDLs inhibit the CRP-induced expression of endothelial cell adhesion proteins.114 The mechanism by which HDLs inhibit the pro-inflammatory effects of CRP appears to be different from that responsible for inhibiting the effects induced by cytokines. Whereas the HDL-mediated inhibition of TNF-–induced expression of endothelial cell adhesion proteins persists for several hours after the HDLs have been removed,100 inhibition of the CRP-induced expression requires the physical presence of HDL during the induction.115 Furthermore, whereas oxidation of HDL reduces the HDL-mediated inhibition of TNF-–induced adhesion protein expression, it enhances the ability of HDL to inhibit the CRP-induced adhesion protein expression.114 It was concluded that the oxidized phospholipids in HDL are more effective than nonoxidized phospholipids in binding and neutralizing the effects of the CRP.114
Relationship Between the Cholesterol Efflux, the Antioxidant, and the Adhesion Molecule Inhibitory Properties of HDL
Both the antioxidant and antiinflammatory properties of HDLs appear to be independent of the cholesterol efflux function of these lipoproteins. The acceptor of the ABCA1-mediated efflux of cholesterol is lipid-free or lipid-poor apoA-I, whereas most of the antioxidant potential of HDL is the consequence of activity of factors, such as paraoxonase that are cotransported with HDL, although there is evidence that both apoA-I and apoA-II also possess at least some intrinsic antioxidant properties.58, 115 The ability of HDL to inhibit the cytokine-induced expression of endothelial cell adhesion molecule (at least in vitro) is achieved as readily (or even more readily) by reconstituted HDL containing only apoA-I and phosphatidylcholine, as by native HDL. Furthermore, whereas lipid-free apoA-I is an effective acceptor of the cholesterol released by the ABCA1-mediated pathway, lipid-free apoA-I does not inhibit endothelial cell adhesion molecule expression. It is likely, therefore, that the cholesterol efflux, the antioxidant, and the antiinflammatory properties of HDL are at least partly independent of each other.
Importance of the Antiinflammatory Effects of HDL In Vivo
The ability of HDL to modify endothelial cell adhesion protein expression has also been demonstrated in vivo. Alternate daily infusions of rHDL containing apoA-I and phosphatidylcholine to apoE–/– mice with carotid peri-arterial collars resulted in 40% reductions in VCAM-1 expression and monocyte infiltration within 1 week and a substantial reduction in the development of neointimal hyperplasia at 3 weeks.116 In another study, a single infusion of rHDL inhibited E-selectin expression in intradermal vessels after subcutaneous administration of IL-1 in a normocholesterolemic porcine model.117 In another study, however, the transgenic expression of human apoA-I on a background of apoE knockout mice had no apparent effect on endothelial VCAM-1 expression, monocyte adherence, or lipid infiltration when studied at an early age.118
There are several reports of the effects of infusing rHDL into humans. In subjects with hypercholesterolemia, a single infusion of rHDL increased flow-mediated dilatation at 4 hours.119 In addition, forearm blood flow measured by venous plethysmography, shown to be impaired in ABCA1 heterozygotes with low plasma HDL, was restored to that of normal controls 4 hours after an infusion of rHDL.120 These studies highlight the ability of a single infusion of rHDL to raise plasma HDL and improve vascular reactivity. These studies, combined with the rapidity of antiatherosclerotic effects of infusing rHDL containing apoA-IMilano (an apoA-I variant that may have enhanced antiatherogenic properties22) into rabbits121 and humans,122 raise the possibility that some of the noncholesterol transport functions of HDL may be of pathophysiological importance.
Clinical Implications of Antioxidant/Antiinflammatory Properties of HDL
To the extent that atherosclerosis is an inflammatory disease that is initiated in part by the presence of oxidized LDL in the artery wall, it is logical to conclude that the antioxidant and antiinflammatory properties of HDL may account for at least part of the antiatherogenic potential of these lipoproteins. To date, however, the evidence, although mounting, is still rather sparse.
There are two reports suggesting that the inflammatory/antiinflammatory properties of HDL are superior to HDL cholesterol concentration in terms of discriminating between those with and without CHD.17,95 It should be emphasized, however, that the group sizes in these studies were small, and the results should be interpreted with caution until confirmed in larger studies.
In more direct studies, it has been shown that infusion of human apoA-I into mice and humans results in LDL becoming resistant to oxidation and less effective in inducing monocyte chemotactic activity in a human artery wall coculture.15 On the basis of other studies in which the oral apoA-I mimetic peptide (D-4F) was administered to apoE-null mice,123,124 it was concluded that the beneficial properties of apoA-I and the apoA-I mimetic peptide are linked both by their ability to reduce lipoprotein lipid oxidation and to enhance reverse cholesterol transport.
A relationship between plasma concentrations of HDL cholesterol and soluble cell adhesion molecules has been reported in humans. In a study of subjects with a wide range of HDL cholesterol concentrations, it was found that the plasma levels of soluble ICAM-1 and soluble E-selectin (but not soluble VCAM-1) were significantly higher in subjects with low HDL levels compared with those with average or high HDL levels.125 Furthermore, the concentration of HDL cholesterol correlated inversely with both soluble ICAM-1 (sICAM-1) and soluble E-selectin (sE-selectin) in the low-HDL subjects but not in those with normal or elevated HDL levels.125 It was also found that the increase in HDL levels induced by treatment with fenofibrate was associated with a significant reduction in the plasma concentrations of sICAM-1 and sE-selectin.125 It is unclear, however, whether the reduction in sICAM and sE-selectin was the consequence of the increase in HDL or a direct antiinflammatory effect of the fibrate on the artery wall.
|
Conclusion |
|---|
|
TopAbstractIntroductionOxidationInflammationConclusionReferences |
|---|
There is no doubt that HDLs have multiple functions beyond their ability to promote the efflux of cholesterol from cells. These noncholesterol transport properties have the clear potential to contribute to the antiatherogenic effects of HDL, although the magnitude and clinical importance of such effects remain to be determined. It will be important to determine how newer therapies designed to raise HDL cholesterol levels impact on the antioxidant and antiinflammatory properties of these lipoproteins. It is highly likely that further research directed at understanding these basic processes will yield new strategies for the prevention and treatment of atherosclerosis.
|
Acknowledgments |
|---|
This work was supported in part by the National Health and Medical Research Council of Australia Program Grant 222722 (P.B., K.A.R.) and USPHS grants HL 30568 (A.M.F., M.N.), HL 34343 (G.M.A.), and the Laubisch, Castera and M. K. Gray Funds at UCLA. S.N. was the recipient of a postgraduate medical scholarship of the National Heart Foundation of Australia. G.M.A., M.N., and A.M.F. are principals in Bruin Pharma.
|
Footnotes |
|---|
Original received July 26, 2004; revision received September 8, 2004; accepted September 14, 2004.
|
References |
|---|
|
TopAbstractIntroductionOxidationInflammationConclusionReferences |
|---|
1. Gordon T, Castelli WP, Hjortland MC, Kannel WB, Dawber TR. High density lipoprotein as a protective factor against coronary heart disease. Am J Med. 1977; 62: 707–714.[CrossRef][Medline] [Order article via Infotrieve]
2. Castelli WP, Garrison RJ, Wilson PW, Abbott RD, Kalousdian S, Kannel WB. Incidence of coronary heart disease and lipoprotein cholesterol levels. The Framingham study. JAMA. 1986; 256: 2835–2838.
3. Barter P, Kastelein J, Nunn A, Hobbs R. High density lipoproteins (HDLs) and atherosclerosis: the unanswered questions. Atherosclerosis. 2003; 168: 195–211.[CrossRef][Medline] [Order article via Infotrieve]
4. Zhang Y, Zanotti I, Reilly MP, Glick JM, Rothblat GH, Rader DJ. Overexpression of apolipoprotein A-I promotes reverse transport of cholesterol from macrophages to feces in vivo. Circulation. 2003; 108: 661–663.
5. Levine DM, Parker TS, Donnelly TM, Walsh A, Rubin AL. In vivo protection against endotoxin by plasma high density lipoprotein. Proc Natl Acad Sci USA. 1993; 90: 12040–12044.
6. Murugesan G, Sa G, Fox PL. High-density lipoprotein stimulates endothelial cell movement by a mechanism distinct from basic fibroblast growth factor. Circ Res. 1994; 74: 1149–1156.
7. Sugatani J, Miwa M, Komiyama Y, Ito S. High-density lipoprotein inhibits the synthesis of platelet-activating factor in human vascular endothelial cells. J Lipid Mediators Cell Signal. 1996; 13: 73–88.[CrossRef][Medline] [Order article via Infotrieve]
8. Epand RM, Stafford A, Leon B, Lock PE, Tytler EM, Segrest JP, Anantharamaiah GM. HDL and apolipoprotein A-I protect erythrocytes against the generation of procoagulant activity. Arterioscler Thromb. 1994; 14: 1775–1783.
9. Fleisher LN, Tall AR, Witte LD, Miller RW, Cannon PJ. Stimulation of arterial endothelial cell prostacyclin synthesis by high density lipoproteins. J Biol Chem. 1982; 257: 6653–6655.
10. Yui Y, Aoyama T, Morishita H, Takahashi M, Takatsu Y, Kawai C. Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I. J Clin Invest. 1988; 82: 803–807.[Medline] [Order article via Infotrieve]
11. Ko Y, Haring R, Stiebler H, Wieczorek AJ, Vetter H, Sachinidis A. High-density lipoprotein reduces epidermal growth factor-induced DNA synthesis in vascular smooth muscle cells. Atherosclerosis. 1993; 99: 253–259.[CrossRef][Medline] [Order article via Infotrieve]
12. Viswambharan H, Ming XF, Zhu S, Hubsch A, Lerch P, Vergeres G, Rusconi S, Yang Z. Reconstituted high-density lipoprotein inhibits thrombin-induced endothelial tissue factor expression through inhibition of RhoA and stimulation of phosphatidylinositol 3-kinase but not Akt/endothelial nitric oxide synthase. Circ Res. 2004; 94: 918–925.
13. O’Connell BJ, Genest J Jr. High-density lipoproteins and endothelial function. Circulation. 2001; 104: 1978–1983.
14. Zeiher AM, Schachinger V. Coronary endothelial vasodilator dysfunction: clinical relevance and therapeutic implications. Z Kardiol. 1994; (83 Suppl 4): 7–14.
15. Navab M, Hama SY, Cooke CJ, Anantharamaiah GM, Chaddha M, Jin L, Subbanagounder G, Faull KF, Reddy ST, Miller NE, Fogelman AM. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: step 1. J Lipid Res. 2000; 41: 1481–1494.
16. Navab M, Hama SY, Anantharamaiah GM, Hassan K, Hough GP, Watson AD, Reddy ST, Sevanian A, Fonarow GC, Fogelman AM. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized LDL: Steps 2 & 3. J Lipid Res. 2000; 41: 1495–1508.
17. Navab M, Hama SY, Hough GP, Subbanagounder G, Reddy ST, Fogelman AM. A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids. J Lipid Res. 2001; 42: 1308–1317.
18. Navab M, Berliner JA, Subbanagounder G, Hama S, Lusis AJ, Castellani LW, Reddy S, Shih D, Shi W, Watson AD, Van Lenten BJ, Vora D, Fogelman AM. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler Thromb Vasc Biol. 2001; 21: 481–488.
19. Navab M, Ananthramaiah GM, Reddy ST, Van Lenten BJ, Ansell BJ, Fonarow GC, Vahabzadeh K, Hama S, Hough G, Kamranpour N, Berliner JA, Lusis AJ, Fogelman AM. The oxidation hypothesis of atherogenesis: the role of oxidized phospholipids and HDL. J Lipid Res. 2004; 45: 993–1007.
20. Barter PJ, Rye K-A. High density lipoproteins and coronary heart disease. Atherosclerosis. 1996; 121: 1–12.[CrossRef][Medline] [Order article via Infotrieve]
21. Barter PJ, Baker PW, Rye K-A. Effect of high-density lipoproteins on the expression of adhesion molecules in endothelial cells. Current Opinion in Lipidology. 2002; 13: 285–288.[CrossRef][Medline] [Order article via Infotrieve]
22. Shah PK, Yano J, Reyes O, Chyu KY, Kaul S, Bisgaier CL, Drake S, Cercek B. High-dose recombinant apolipoproteins A-IMilano mobilizes tissue cholesterol and rapidly reduces plaque lipid and macrophage content in apolipoprotein E-deficient mice: potential implications for acute plaque stabilization. Circulation. 2001; 103: 3047–3050.
23. Hessler JR, Robertson AL, Chisolm GM. LDL-induced cytotoxicity and its inhibition by HDL in human vascular smooth muscle and endothelial cells in culture. Atherosclerosis. 1979; 32: 213–229.[CrossRef][Medline] [Order article via Infotrieve]
24. Fogelman AM, Shechter I, Seager J, Hokom M, Child JS, Edwards PA. Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages. Proc Natl Acad Sci U S A. 1980; 77: 2214–2218.
25. Henricksen T, Mahoney EM, Steinberg D. Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: recognition by receptor for acetylated low density lipoproteins. Proc Natl Acad Sci U S A. 1981; 78: 6499–6503.
26. Parthasarathy S. Modified Lipoproteins in the Pathogenesis of Atherosclerosis. Austin, TX: RG Landes Co; 1994: 91–119.
27. Nievelstein PF, Fogelman AM, Mottino G, Frank JS. Lipid accumulation in rabbit aortic intima two hours after bolus infusion of low density lipoprotein: A deep-etch and immuno-localization study of ultra-rapidly frozen tissue. Arterioscler Thromb. 1991; 11: 1795–1805.
28. Tsimikas S, Lau HK, Han K-R, et al. Percutaneous coronary intervention results in acute increases in oxidized phospholipids and lipoprotein(a). Short-term and long-term immunologic responses to oxidized low-density lipoprotein. Circulation. 2004. In press.
29. Cyrus T, Pratico D, Zhao L, Witztum JL, Rader DJ, Rokach J, FitzGerald GA, Funk CD. Absence of 12/15-lipoxygenase expression decreases lipid peroxidation and atherogenesis in apolipoprotein E–deficient mice. Circulation. 2001; 103: 2277–2282.
30. George J, Afek A, Shaish A, Levkovitz H, Bloom N, Cyrus T, Zhao L, Funk CD, Sigal E, Harats D. 12/15-lipoxygenase gene disruption attenuates atherogenesis in LDL receptor–deficient mice. Circulation. 2001; 104: 1646–1650.
31. Zhao L, Cuff CA, Moss e, Wille U, Cyrus T, Klein EA, Pratico D, Rader DJ, Hunter CA, Pure E, Funk CD. Selective interleukin-12 synthesis defect in 12/15-lipoxygenase deficient macrophages associated with reduced atherosclerosis in a mouse model of familial hypercholesterolemia. J Biol Chem. 2002; 277: 35350–35356.
32. Harats D, Shaish A, George J, Mulkins M, Kurihara H, Levkovitz H, Sigal E. Overexpression of 15-lipoxygenase in vascular endothelium accelerates early atherosclerosis in LDL receptor-deficient mice. Arterioscler Thromb Vasc Biol. 2000; 20: 2100–2105.
33. Reilly KB, Srinivasan S, Hatley ME, Patricia MK, Lannigan J, Bolick DT, Vandenhoff G, Pei H, Natarajan R, Nadler JL, Hedrick CC. 12/15 Lipoxygenase Activity Mediates Inflammatory Monocyte: Endothelial Interactions and Atherosclerosis In Vivo. J Biol Chem. 2004; 279: 9440–9450.
34. Mehrabian M, Allayee H, Wong J, Shi W, Wang XP, Shaposhnik Z, Funk CD, Lusis AJ, Shih W. Identification of 5-lipoxygenase as a major gene contributing to atherosclerosis susceptibility in mice. Circ Res. 2002; 91: 120–126.
35. Mehrabian M, Allayee H. 5-lipoxygenase and atherosclerosis. Curr Opin Lipidol. 2003; 14: 447–457.[CrossRef][Medline] [Order article via Infotrieve]
36. Dwyer JH, Allayee H, Dwyer KM, Fan J, Wu H, Mar R, Lusis AJ, Mehrabian M. Arachidonate 5-lipoxygenase promoter genotype, dietary arachidonic acid, and atherosclerosis. N Engl J Med. 2004; 350: 29–37.
37. Thukkani AK, McHowat J, Hsu FF, Brennan ML, Hazen SL, Ford DA. Identification of -chloro fatty aldehydes and unsaturated lysophosphatidylcholine molecular species in human atherosclerotic lesions. Circulation. 2003; 108: 3128–3133.
38. Carr AC, McCall MR, Frei B. Oxidation of LDL by myeloperoxidase and reactive nitrogen species oxidation of LDL by myeloperoxidase and reactive nitrogen species. Arterioscler Thromb Vasc Biol. 2000; 20: 1716–1723.
39. Zhang R, Brennan ML, Shen Z, MacPherson JC, Schmitt D, Molenda CE, Hazen SL. Myeloperoxidase functions as a major enzymatic catalyst for initiation of lipid peroxidation at sites of inflammation. J Biol Chem. 2002; 277: 46116–46122.
40. Shishehbor MH, Aviles RJ, Brennan ML, Fu X, Goormastic M, Pearce GL, Gokce N, Keaney JF Jr., Penn MS, Sprecher DL, Vita JA, Hazen SL. Association of nitrotyrosine levels with cardiovascular disease and modulation by statin therapy. JAMA. 2003; 289: 1675–1680.
41. Brennan ML, Penn MS, Van Lente F, Nambi V, Shishehbor MH, Aviles RJ, Goormastic M, Pepoy ML, McErlean ES, Topol EJ, Nissen SE, Hazen SL, Prognostic value of myeloperoxidase in patients with chest pain. N Engl J Med. 2003; 349: 1595–1604.
42. Brennan M-L, Hazen SL. Emerging role of myeloperoxidase and oxidant stress markers in cardiovascular risk assessment. Curr Opin Lipidol. 2003; 14: 353–359.[CrossRef][Medline] [Order article via Infotrieve]
43. Gaut JP, Byun J, Tran HD, Lauber WM, Carroll JA, Hotchkiss RS, Belaaouaj A, Heinecke JW. Myeloperoxidase produces nitrating oxidants in vivo. J Clin Invest. 2002; 109: 1311–1319.[CrossRef][Medline] [Order article via Infotrieve]
44. Linton MF, Fazio S. Cyclooxygenase-2 and inflammation in atherosclerosis. Curr Opin Pharmacol. 2004; 4: 116–123.[CrossRef][Medline] [Order article via Infotrieve]
45. Natarajan R, Nadler JL. Lipid inflammatory mediators in diabetic vascular disease. Arterioscler Thromb Vasc Biol. 2004; 24: 1542–1548.
46. Vila L. Cyclooxygenase and 5-lipoxygenase pathways in the vessel wall: Role in atherosclerosis. Med Res Rev. 2004; 24: 399–424.[CrossRef][Medline] [Order article via Infotrieve]
47. Sorescu D, Szocs K, Griendling KK. NAD(P)H oxidases and their relevance to atherosclerosis. Trends Cardiovasc Med. 2001; 11: 124–131.[CrossRef][Medline] [Order article via Infotrieve]
48. Cathcart MK. Regulation of superoxide anion production by NADPH oxidase in monocytes/macrophages. Contributions to atherosclerosis. Arterioscler Thromb Vasc Biol. 2004; 24: 23–28.
49. Lee SH, Oe T, Blair IA. Vitamin C-induced decomposition of lipid hydroperoxides to endogenous genotoxins. Science. 2001; 292: 2083–2086.
50. Oe T, Lee SH, Silva Elipe MV, Arison BH, Blair IA. A novel lipid hydroperoxide-derived modification to arginine. Chem Res Toxicol. 2003; 16: 1598–1605.[CrossRef][Medline] [Order article via Infotrieve]
51. Christison J, Karjalainen A, Brauman J, Bygrave F, Stocker R. Rapid reduction and removal of HDL- but not LDL-associated cholesteryl ester hydroperoxides by rat liver perfused in situ. Biochem J. 1996; 314: 739–742.[Medline] [Order article via Infotrieve]
52. Sattler W, Stocker R. Greater selective uptake by Hep G2 cells of high-density lipoprotein cholesteryl ester hydroperoxides than of unoxidized cholesteryl esters. Biochem J. 1993; 294: 771–778.[Medline] [Order article via Infotrieve]
53. Bowry VW, Stanley KK, Stocker R. High density lipoprotein is the major carrier of lipid hydroperoxides in human blood plasma from fasting donors. Proc Natl Acad Sci U S A. 1992; 89: 10316–10320.
54. Mackness B, Hine D, Liu Y, Mastorikou M, Mackness M. Paraoxonase-1 inhibits oxidized LDL-induced MCP-1 production by endothelial cells. Biochem Biophys Res Commun. 2004; 318: 680–683.[CrossRef][Medline] [Order article via Infotrieve]
55. Shih D.M., Xia Y. -R., Wang X-P., Miller E., Castellani L.W., Subbanagounder G., Cheroutre H., Faull K., Berliner J.A., Witztum J.L., Lusis A.J. Combined serum paraoxonase/apolipoprotein E knockout mice exhibit increased lipoprotein oxidation and atherosclerosis. J Biol Chem. 2000; 275: 17527–17535.
56. Tward A, Xia YR, Wang XP, Shi YS, Park C, Castellani LW, Lusis AJ, Shih DM. Decreased atherosclerotic lesion formation in human serum paraoxonase transgenic mice. Circulation. 2002; 106: 484–490.
57. Reddy ST, Wadleigh DJ, Grijalva V, Ng C, Hama S, Gangopadhyay A, Shih DM, Lusis AJ, Navab M, Fogelman AM. Human paraoxonase-3 is an HDL-associated enzyme with biological activity similar to paraoxonase-1 protein but is not regulated by oxidized lipids. Arterioscler Thromb Vasc Biol. 2001; 21: 542–547.
58. Garner B, Waldeck AR, Witting PK, Rye KA, Stocker R. Oxidation of high density lipoproteins. II. Evidence for direct reduction of lipid hydroperoxides by methionine residures of apolipoproteins AI and AII. J Biol Chem. 1998; 273: 6088–6095.
59. Watson AD, Navab M, Hama SY, Sevanian A, Prescott SM, Stafforini DM, McIntyre TM, Du BN, Fogelman AM, Berliner JA. Effect of platelet activating factor-acetylhydrolase on the formation and action of minimally oxidized-low density lipoprotein. J Clin Invest. 1995; 95: 774–782.[Medline] [Order article via Infotrieve]
60. Forte TM, Subbanagounder G, Berliner JA, Blanche PJ, Clermont AO, Jia Z, Oda MN, Krauss RM, Bielicki JK. Altered activities of anti-atherogenic enzymes LCAT, paraoxonase, and platelet-activating factor acetylhydrolase in atherosclerosis-susceptible mice. J Lipid Res. 2002; 43: 477–485.
61. Singh IP, Baron S. Innate defences against viremia. Rev Med Virol. 2000; 10: 395–403.[CrossRef][Medline] [Order article via Infotrieve]
62. Van Lenten BJ, Wagner AC, Nayak DP, Hama S, Navab M, Fogelman AM. High-density lipoprotein loses its anti-inflammatory properties during acute influenza A infection. Circulation. 2001; 103: 2283–2288.
63. Van Lenten BJ, Wagner AC, Anantharamaiah GM, Garber DW, Fishbein MC, Adhikary L, Nayak DP, Hama S, Navab M, Fogelman AM. Influenza infection promotes macrophage traffic into arteries of mice that is prevented by D-4F, an apolipoprotein A-I mimetic peptide. Circulation. 2002; 106: 1127–1132.
64. Burger D, Dayer J-M. High-density lipoprotein-associated apolipoprotein A-I: the missing link between infection and chronic inflammation? Autoimmunity Rev. 2002; 1: 111–117.
65. Van Lenten BJ, Wagner AC, Navab M, Anantharamaiah GM, Ka-Wai Hui, E, Nayak DP, Fogelman AM. D-4F, an ApoA-I Mimetic Peptide, Inhibits the Inflammatory Response Induced by Influenza A Infection of Human Type II Pneumocytes. Circulation. 2004. In press.
66. Osterud B, Bjorklid E. Role of monocytes in atherogenesis. Physiol Rev. 2003; 83: 1069–1112.
67. Davenport P, Tipping PG. The role of interleukin-4 and interleukin-12 in the progression of atherosclerosis in apolipoprotein E-deficient mice. Am J Pathol. 2003; 163: 1117–1125.
68. Ridker PM. On evolutionary biology, inflammation, infection, and the causes of atherosclerosis. Circulation. 2002; 105: 2–4.
69. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002; 105: 1135–1143.
70. Libby P, Ridker PM. Inflammation and atherosclerosis: role of C-reactive protein in risk assessment. Am J Med. 2004; 116 (Suppl 6A): 9S–16S.[CrossRef][Medline] [Order article via Infotrieve]
71. Shih PT, Elices MJ, Fang ZT, Ugarova TP, Strahl D, Territo MC, Frank JS, Kovach NL, Cabanas C, Berliner JA, Vora DK. Minimally modified low-density lipoprotein induces monocyte adhesion to endothelial connecting segment-1 by activating beta integrin. J Clin Invest. 1999; 103: 613–625.[Medline] [Order article via Infotrieve]
72. Carlos TM, Schwartz BR, Kovach NL, Yee E, Rosa M, Osborn L, Chi-Rosso G, Newman B, Lobb R, Rosa M. Vascular cell adhesion molecule-1 mediates lymphocyte adherence to cytokine-activated cultured human endothelial cells. Blood. 1990; 76: 965–970.
73. Blankenberg S, Barbaux S, Tiret L. Adhesion molecules and atherosclerosis. Atherosclerosis. 2003; 170: 191–203.[CrossRef][Medline] [Order article via Infotrieve]
74. O’Brien KD, McDonald TO, Chait A, Allen MD, Alpers CE. Neovascular expression of E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in human atherosclerosis and their relation to intimal leukocyte content. Circulation. 1996; 93: 672–682.
75. Lawrence MB, Springer TA. Leukocytes roll on a selectin at physiologic flow rates: distinction from and prerequisite for adhesion through integrins. Cell. 1991; 65: 859–873.[CrossRef][Medline] [Order article via Infotrieve]
76. Davies MJ, Gordon JL, Gearing AJ, Pigott R, Woolf N, Katz D, Kyriakopoulos A. The expression of the adhesion molecules ICAM-1, VCAM-1, PECAM, and E-selectin in human atherosclerosis. J Pathol. 1993; 171: 223–229.[CrossRef][Medline] [Order article via Infotrieve]
77. Springer TA. Adhesion receptors of the immune system. Nature. 1990; 346: 425–434.[CrossRef][Medline] [Order article via Infotrieve]
78. Kume N, Cybulsky MI, Gimbrone Jr MA. Lysophosphatidylcholine, a component of atherogenic lipoproteins, induces mononuclear leukocyte adhesion molecules in cultured human and rabbit arterial endothelial cells. J Clin Invest. 1992; 90: 1138–1144.[Medline] [Order article via Infotrieve]
79. Li H, Cybulsky MI, Gimbrone MA, Jr., Libby P. An atherogenic diet rapidly induces VCAM-1, a cytokine-regulatable mononuclear leukocyte adhesion molecule, in rabbit aortic endothelium. Arterioscler Thromb. 1993; 13: 197–204.
80. Walpola PL, Gotlieb AI, Cybulsky MI, Langille BL. Expression of ICAM-1 and VCAM-1 and monocyte adherence in arteries exposed to altered shear stress. Arterioscler Thromb Vasc Biol. 1995; 15: 2–10.
81. Krejcy K, Schwarzacher S, Ferber W, Plesch C, Cybulsky MI, Weidinger FF. Expression of VCAM-1 in rabbit iliac arteries is associated with vasodilator dysfunction of regenerated endothelium following balloon injury. Atherosclerosis. 1996; 122: 59–67.[CrossRef][Medline] [Order article via Infotrieve]
82. Auer J, Weber T, Berent R, Lassnig E, Lamm G, Eber B. Genetic polymorphisms in cytokine and adhesion molecule genes in coronary artery disease. Am J Pharmacogenomics. 2003; 3: 317–328.[CrossRef][Medline] [Order article via Infotrieve]
83. Dansky HM, Barlow CB, Lominska C, Sikes JL, Kao C, Weinsaft J, Cybulsky MI, Smith JD. Adhesion of monocytes to arterial endothelium and initiation of atherosclerosis are critically dependent on vascular cell adhesion molecule-1 gene dosage. Arterioscler Thromb Vasc Biol. 2001; 21: 1662–1667.
84. Oguchi S, Dimayuga P, Zhu J, Chyu KY, Yano J, Shah PK, Nilsson J, Cercek B. Monoclonal antibody against vascular cell adhesion molecule-1 inhibits neointimal formation after periadventitial carotid artery injury in genetically hypercholesterolemic mice. Arterioscler Thromb Vasc Biol. 2000; 20: 1729–1736.
85. Lumsden AB, Chen C, Hughes JD, Kelly AB, Hanson SR, Harker LA. Anti-VLA-4 antibody reduces intimal hyperplasia in the endarterectomized carotid artery in nonhuman primates. J Vasc Surg. 1997; 26: 87–93.[CrossRef][Medline] [Order article via Infotrieve]
86. Mach F, Schonbeck U, Sukhova GK, Atkinson E, Libby P. Reduction of atherosclerosis in mice by inhibition of CD40 signalling. Nature. 1998; 394: 200–203.[CrossRef][Medline] [Order article via Infotrieve]
87. Bourdillon MC, Poston RN, Covacho C, Chignier E, Bricca G, McGregor JL. ICAM-1 deficiency reduces atherosclerotic lesions in double-knockout mice (ApoE(–/–)/ICAM-1(–/–) fed a fat or a chow diet. Arterioscler Thromb Vasc Biol. 2000; 20: 2630–2635.
88. Cybulsky MI, Iiyama K, Li H, Zhu S, Chen M, Iiyama M, Davis V, Gutierrez-Ramos JC, Connelly PW, Milstone DS. A major role for VCAM-1, but not ICAM-1, in early atherosclerosis. J Clin Invest. 2001; 107: 1255–1262.[Medline] [Order article via Infotrieve]
89. Hwang SJ, Ballantyne CM, Sharrett AR, Smith LC, Davis CE, Gotto AM Jr., Boerwinkle E. Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases. The atherosclerosis risk in communities (ARIC) study. Circulation. 1997; 96: 4219–4225.
90. Blankenberg S, Rupprecht HJ, Bickel C, Peetz D, Hafner G, Tiret L, Meyer J. Circulating cell adhesion molecules and death in patients with coronary artery disease. Circulation. 2001; 104: 1336–1342.
91. Reape TJ, Groot PH. Chemokines and atherosclerosis. Atherosclerosis. 1999; 147: 213–225.[CrossRef][Medline] [Order article via Infotrieve]
92. Navab M, Imes SS, Hama SY, Hough GP, Ross LA, Bork RW, Valente AJ, Berliner JA, Drinkwater DC, Laks H. Monocyte transmigration induced by modification of low density lipoprotein in cocultures of human aortic wall cells is due to induction of monocyte chemotactic protein 1 synthesis and is abolished by high density lipoprotein. J Clin Invest. 1991; 88: 2039–2046.[Medline] [Order article via Infotrieve]
93. Van Lenten BJ, Hama SY, de Beer FC, Stafforini DM, McIntyre TM, Prescott SM, La Du BN, Fogelman AM, Navab M. Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures. J Clin Invest. 1995; 96: 2758–2767.[Medline] [Order article via Infotrieve]
94. Ashby D, Gamble J, Vadas M, Fidge N, Siggins S, Rye K, Barter PJ. Lack of effect of serum amyloid A (SAA) on the ability of high-density lipoproteins to inhibit endothelial cell adhesion molecule expression. Atherosclerosis. 2001; 154: 113–121.[CrossRef][Medline] [Order article via Infotrieve]
95. Ansell BJ, Navab M, Hama S, Kamranpour N, Fonarow G, Hough G, Rahmani S, Mottahedeh R, Dave R, Reddy ST, Fogelman AM. Inflammatory/Antiinflammatory Properties of High-Density Lipoprotein Distinguish Patients From Control Subjects Better Than High-Density Lipoprotein Cholesterol Levels and Are Favorably Affected by Simvastatin Treatment. Circulation. 2003; 108: 2751–2756.
96. Cockerill GW, Rye KA, Gamble JR, Vadas MA, Barter PJ. High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler Thromb Vasc Biol. 1995; 15: 1987–1994.
97. Calabresi L, Franceschini G, Sirtori CR, De Palma A, Saresella M, Ferrante P, Taramelli D. Inhibition of VCAM-1 expression in endothelial cells by reconstituted high density lipoproteins. Biochem Biophys Res Commun. 1997; 238: 61–65.[CrossRef][Medline] [Order article via Infotrieve]
98. Park SH, Park JH, Kang JS, Kang YH. Involvement of transcription factors in plasma HDL protection against TNF-alpha-induced vascular cell adhesion molecule-1 expression. Int J Biochem Cell Biol. 2003; 35: 168–182.[CrossRef][Medline] [Order article via Infotrieve]
99. Xia P, Vadas MA, Rye KA, Barter PJ, Gamble JR. High density lipoproteins (HDL) interrupt the sphingosine kinase signaling pathway. A possible mechanism for protection against atherosclerosis by HDL. J Biol Chem. 1999; 274: 33143–33147.
100. Clay MA, Pyle DH, Rye K-A, Vadas MA, Gamble JR, Barter PJ. Time sequence of the inhibition of endothelial adhesion molecule expression by reconstituted high density lipoproteins. Atherosclerosis,. 2001; 157: 23–29.[CrossRef][Medline] [Order article via Infotrieve]
101. Ashby DT, Rye K-A, Clay MA., Vadas MA, Gamble J, Barter PJ. Factors influencing the ability of HDL to inhibit expression of vascular cell adhesion molecule-1 in endothelial cells. Arterioscler Thromb Vasc Biol. 1998; 18: 1450–1455.
102. Baker PW, Rye K-A, Gamble JR, Vadas MA, Barter PJ. Ability of reconstituted high density lipoproteins to inhibit cytokine-induced expression of vascular cell adhesion molecule-1 in human umbilical cell endothelial cells. J Lipid Res. 1999; 40: 345–353.
103. Baker PW, Rye KA, Gamble JR, Vadas MA, Barter PJ. Phospholipid composition of reconstituted high density lipoproteins influences their ability to inhibit endothelial cell adhesion molecule expression. J Lipid Res. 2000; 41: 1261–1267.
104. De Caterina R, Bernini W, Carluccio MA, Liao JK, Libby P. Structural requirements for inhibition of cytokine-induced endothelial activation by unsaturated fatty acids. J Lipid Res. 1998; 39: 1062–1070.
105. Stannard AK, Khan S, Graham A, Owen JS, Allen SP. Inability of plasma high-density lipoproteins to inhibit cell adhesion molecule expression in human coronary artery endothelial cells. Atherosclerosis. 2001; 154: 31–38.[CrossRef][Medline] [Order article via Infotrieve]
106. Zhang WJ, Stocker R, McCall MR, Forte TM, Frei B. Lack of inhibitory effect of HDL on TNFalpha-induced adhesion molecule expression in human aortic endothelial cells. Atherosclerosis. 2002; 165: 241–249.[CrossRef][Medline] [Order article via Infotrieve]
107. Cockerill GW, Saklatvala J, Ridley SH, Yarwood H, Miller NE, Oral B, Nithyanathan S, Taylor G, Haskard DO. High-density lipoproteins differentially modulate cytokine-induced expression of E-selectin and cyclooxygenase-2. Arterioscler Thromb Vasc Biol. 1999; 19: 910–917.
108. Matsunaga T, Hokari S, Koyama I, Harada T, Komoda T NF-kappa B activation in endothelial cells treated with oxidized high-density lipoprotein. Biochem Biophys Res Commun. 2003; 303: 313–319.[CrossRef][Medline] [Order article via Infotrieve]
109. Robbesyn F, Garcia V, Auge N, Vieira O, Frisach MF, Salvayre R, Negre-Salvayre A. HDL counterbalance the proinflammatory effect of oxidized LDL by inhibiting intracellular reactive oxygen species rise, proteasome activation, and subsequent NF-kappaB activation in smooth muscle cells. FASEB J. 2003; 17: 743–745.
110. Rong JX, Li J, Reis ED, Choudhury RP, Dansky HM, Elmalem VI, Fallon JT, Breslow JL, Fisher EA. Elevating high-density lipoprotein cholesterol in apolipoprotein E-deficient mice remodels advanced atherosclerotic lesions by decreasing macrophage and increasing smooth muscle cell content. Circulation. 2001; 104: 2447–2452.
111. Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation. 2000; 102: 2165–2168.
112. Pasceri V, Cheng JS, Willerson JT, Yeh ET, Chang J. Modulation of C-reactive protein-mediated monocyte chemoattractant protein-1 induction in human endothelial cells by anti-atherosclerosis drugs. Circulation. 2001; 103: 2531–2534.
113. Venugopal SK, Devaraj S, Yuhanna I, Shaul P, Jialal I. Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation. 2002; 106: 1439–1441.
114. Wadham C, Albanese N, Roberts J, Wang L, Bagley CJ, Gamble JR, Rye KA, Barter PJ, Vadas MA, Xia P. High-density lipoproteins neutralize C-reactive protein inflammatory activity. Circulation. 2004; 109: 2116–2122.
115. Garner B, Witting PK, Waldeck AR, Christison JK, Raftery M, Stocker R. Oxidation of high density lipoproteins. I. Formation of methionine sulfoxide in apolipoproteins AI and AII is an early event that accompanies lipid peroxidation and can be enhanced by alpha-tocopherol. J Biol Chem. 1998; 273: 6080–6087.
116. Dimayuga P, Zhu J, Oguchi S, Chyu KY, Xu XO, Yano J, Shah PK, Nilsson J, Cercek B. Reconstituted HDL containing human apolipoprotein A-1 reduces VCAM-1 expression and neointima formation following periadventitial cuff-induced carotid injury in apoE null mice. Biochem Biophys Res Commun. 1999; 264: 465–468.[CrossRef][Medline] [Order article via Infotrieve]
117. Cockerill GW, Huehns TY, Weerasinghe A, Stocker C, Lerch PG, Miller NE, Haskard DO. Elevation of plasma high-density lipoprotein concentration reduces interleukin-1-induced expression of E-selectin in an in vivo model of acute inflammation. Circulation. 2001; 103: 108–112.
118. Dansky HM, Charlton SA, Barlow CB, Tamminen M, Smith JD, Frank JS, Breslow JL. Apo A-I inhibits foam cell formation in Apo E-deficient mice after monocyte adherence to endothelium. J Clin Invest. 1999; 104: 31–39.[Medline] [Order article via Infotrieve]
119. Spieker LE, Sudano I, Hurlimann D, Lerch PG, Lang MG, Binggeli C, Corti R, Ruschitzka F, Luscher TF, Noll G. High-density lipoprotein restores endothelial function in hypercholesterolemic men. Circulation. 2002; 105: 1399–1402.
120. Bisoendial RJ, Hovingh GK, Levels JH, Lerch PG, Andresen I, Hayden MR, Kastelein JJ, Stroes ES. Restoration of endothelial function by increasing high-density lipoprotein in subjects with isolated low high-density lipoprotein. Circulation. 2003; 107: 2944–2948.
121. Chiesa G, Monteggia E, Marchesi M, Lorenzon P, Laucello M, Lorusso V, Di Mario C, Karvouni E, Newton RS, Bisgaier CL, Franceschini G, Sirtori CR. Recombinant apolipoprotein A-I(Milano) infusion into rabbit carotid artery rapidly removes lipid from fatty streaks. Circ Res. 2002; 90: 974–980.
122. Nissen SE, Tsunoda T, Tuzcu EM, Schoenhagen P, Cooper CJ, Yasin M, Eaton GM, Lauer MA, Sheldon WS, Grines CL, Halpern S, Crowe T, Blankenship JC, Kerensky R. Effect of recombinant apoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes. A randomized controlled trial. JAMA. 2003; 290: 2292–2300.
123. Navab M, Anantharamaiah GM, Hama S, Garber DW, Chaddha M, Hough G, Lallone R, Fogelman AM. Oral administration of an apoA-I mimetic peptide synthesized from D-amino acids dramatically reduces atherosclerosis in mice independent of plasma cholesterol. Circulation. 2002; 105: 290–292.
124. Navab M, Anantharamaiah GM, Reddy ST, Hama S, Hough G, Grijalva VR, Wagner AC, Frank JS, Datta G, Garber D, Fogelman AM. Oral D-4F causes formation of pre-ß high-density lipoprotein and improves high-density lipoprotein-mediated cholesterol efflux and reverse cholesterol transport from macrophages in apolipoproteinE-null mice. Ciruclation. 2004; 109: r120–r125.
125. Calabresi L, Gomaraschi M, Villa B, Omoboni L, Dmitrieff C, Franceschini G. Elevated cellular adhesion molecules in subjects with low HDL-cholesterol. Arterioscler Thromb Vasc Biol. 2002; 22: 656–661.
This article has been cited by other articles:
 |
|
 |
|
  D. De Keyzer, S.-A. Karabina, W. Wei, B. Geeraert, D. Stengel, J. Marsillach, J. Camps, P. Holvoet, and E. Ninio Increased PAFAH and Oxidized Lipids Are Associated With Inflammation and Atherosclerosis in Hypercholesterolemic Pigs Arterioscler Thromb Vasc Biol, December 1, 2009; 29(12): 2041 - 2046. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Undurti, Y. Huang, J. A. Lupica, J. D. Smith, J. A. DiDonato, and S. L. Hazen Modification of High Density Lipoprotein by Myeloperoxidase Generates a Pro-inflammatory Particle J. Biol. Chem., November 6, 2009; 284(45): 30825 - 30835. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. A. Grover, M. Kaouache, L. Joseph, P. Barter, and J. Davignon Evaluating the Incremental Benefits of Raising High-Density Lipoprotein Cholesterol Levels During Lipid Therapy After Adjustment for the Reductions in Other Blood Lipid Levels Arch Intern Med, October 26, 2009; 169(19): 1775 - 1780. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. N. Hoofnagle and J. W. Heinecke Lipoproteomics: using mass spectrometry-based proteomics to explore the assembly, structure, and function of lipoproteins J. Lipid Res., October 1, 2009; 50(10): 1967 - 1975. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. T. Bloomgarden The 6th Annual World Congress on the Insulin Resistance Syndrome Diabetes Care, October 1, 2009; 32(10): e114 - e121. [Full Text] [PDF]
|
|
|
|
 |
|
 K. J.E. Sattler, J. Herrmann, S. Yun, N. Lehmann, Z. Wang, G. Heusch, S. Sack, R. Erbel, and B. Levkau High high-density lipoprotein-cholesterol reduces risk and extent of percutaneous coronary intervention-related myocardial infarction and improves long-term outcome in patients undergoing elective percutaneous coronary intervention Eur. Heart J., August 1, 2009; 30(15): 1894 - 1902. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Vaisar Thematic Review Series: Proteomics. Proteomic analysis of lipid-protein complexes J. Lipid Res., May 1, 2009; 50(5): 781 - 786. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Proudfoot, A. E. Barden, W. M. Loke, K. D. Croft, I. B. Puddey, and T. A. Mori HDL is the major lipoprotein carrier of plasma F2-isoprostanes J. Lipid Res., April 1, 2009; 50(4): 716 - 722. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Shao and J. W. Heinecke HDL, lipid peroxidation, and atherosclerosis J. Lipid Res., April 1, 2009; 50(4): 599 - 601. [Full Text] [PDF]
|
|
|
|
 |
|
 H. Otera, T. Ishida, T. Nishiuma, K. Kobayashi, Y. Kotani, T. Yasuda, R. K. Kundu, T. Quertermous, K.-i. Hirata, and Y. Nishimura Targeted inactivation of endothelial lipase attenuates lung allergic inflammation through raising plasma HDL level and inhibiting eosinophil infiltration Am J Physiol Lung Cell Mol Physiol, April 1, 2009; 296(4): L594 - L602. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. W. Heinecke The HDL proteome: a marker-and perhaps mediator-of coronary artery disease J. Lipid Res., April 1, 2009; 50(Supplement): S167 - S171. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. S. Wang, B. Shao, M. N. Oda, J. W. Heinecke, S. Mahler, and R. Stocker A sensitive and specific ELISA detects methionine sulfoxide-containing apolipoprotein A-I in HDL J. Lipid Res., March 1, 2009; 50(3): 586 - 594. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-i. Chen, S.-L. Kao, M.-H. Tsai, M.-S. Shiao, and C. J. Jen Exercise Training Modulates the Effects of Lipoproteins on Acetylcholine-Induced Endothelial Calcium Signaling in Rat Aortas Experimental Biology and Medicine, March 1, 2009; 234(3): 323 - 331. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-P. Despres, R. Ross, G. Boka, N. Almeras, I. Lemieux, and for the ADAGIO-Lipids Investigators Effect of Rimonabant on the High-Triglyceride/ Low-HDL-Cholesterol Dyslipidemia, Intraabdominal Adiposity, and Liver Fat: The ADAGIO-Lipids Trial Arterioscler Thromb Vasc Biol, March 1, 2009; 29(3): 416 - 423. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Jahangiri, M. C. de Beer, V. Noffsinger, L. R. Tannock, C. Ramaiah, N. R. Webb, D. R. van der Westhuyzen, and F. C. de Beer HDL Remodeling During the Acute Phase Response Arterioscler Thromb Vasc Biol, February 1, 2009; 29(2): 261 - 267. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Lu, M. E. T. Dolle, S. Imholz, R. van 't Slot, W. M. M. Verschuren, C. Wijmenga, E. J. M. Feskens, and J. M. A. Boer Multiple genetic variants along candidate pathways influence plasma high-density lipoprotein cholesterol concentrations J. Lipid Res., December 1, 2008; 49(12): 2582 - 2589. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W.-Y. Zhang, E. A. Schwartz, P. A. Permana, and P. D. Reaven Pioglitazone Inhibits the Expression of Inflammatory Cytokines From Both Monocytes and Lymphocytes in Patients With Impaired Glucose Tolerance Arterioscler Thromb Vasc Biol, December 1, 2008; 28(12): 2312 - 2318. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Kimura, C. Mogi, H. Tomura, A. Kuwabara, D.-S. Im, K. Sato, H. Kurose, M. Murakami, and F. Okajima Induction of Scavenger Receptor Class B Type I Is Critical for Simvastatin Enhancement of High-Density Lipoprotein-Induced Anti-Inflammatory Actions in Endothelial Cells J. Immunol., November 15, 2008; 181(10): 7332 - 7340. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. Regieli, J. W. Jukema, D. E. Grobbee, J. J.P. Kastelein, J. A. Kuivenhoven, A. H. Zwinderman, Y. van der Graaf, M. L. Bots, and P. A. Doevendans CETP genotype predicts increased mortality in statin-treated men with proven cardiovascular disease: an adverse pharmacogenetic interaction Eur. Heart J., November 2, 2008; 29(22): 2792 - 2799. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. K. Schnoes, I. Z. Jaffe, L. Iyer, A. Dabreo, M. Aronovitz, B. Newfell, U. Hansen, G. Rosano, and M. E. Mendelsohn Research Resource: Rapid Recruitment of Temporally Distinct Vascular Gene Sets by Estrogen Mol. Endocrinol., November 1, 2008; 22(11): 2544 - 2556. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. Murphy, K. J. Woollard, A. Hoang, N. Mukhamedova, R. A. Stirzaker, S. P.A. McCormick, A. T. Remaley, D. Sviridov, and J. Chin-Dusting High-Density Lipoprotein Reduces the Human Monocyte Inflammatory Response Arterioscler Thromb Vasc Biol, November 1, 2008; 28(11): 2071 - 2077. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D J Hausenloy and D M Yellon Targeting residual cardiovascular risk: raising high-density lipoprotein cholesterol levels Postgrad. Med. J., November 1, 2008; 84(997): 590 - 598. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Nicholls The Complex Intersection of Inflammation and Oxidation: Implications for Atheroprotection J. Am. Coll. Cardiol., October 21, 2008; 52(17): 1379 - 1380. [Full Text] [PDF]
|
|
|
|
|
|
N. J. Hime, A. S. Black, J. J. Bulgrien, and L. K. Curtiss Leukocyte-derived hepatic lipase increases HDL and decreases en face aortic atherosclerosis in LDLr-/- mice expressing CETP J. Lipid Res., October 1, 2008; 49(10): 2113 - 2123. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. S. Green, T. Vaisar, S. Pennathur, J. J. Kulstad, A. B. Moore, S. Marcovina, J. Brunzell, R. H. Knopp, X.-Q. Zhao, and J. W. Heinecke Combined Statin and Niacin Therapy Remodels the High-Density Lipoprotein Proteome Circulation, September 16, 2008; 118(12): 1259 - 1267. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Shao, G. Cavigiolio, N. Brot, M. N. Oda, and J. W. Heinecke Methionine oxidation impairs reverse cholesterol transport by apolipoprotein A-I PNAS, August 26, 2008; 105(34): 12224 - 12229. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Pirillo, P. Uboldi, C. Bolego, H. Kuhn, and A. L. Catapano The 15-Lipoxygenase-Modified High Density Lipoproteins 3 Fail to Inhibit the TNF-{alpha}-Induced Inflammatory Response in Human Endothelial Cells J. Immunol., August 15, 2008; 181(4): 2821 - 2830. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Tolle, A. Pawlak, M. Schuchardt, A. Kawamura, U. J. Tietge, S. Lorkowski, P. Keul, G. Assmann, J. Chun, B. Levkau, et al. HDL-Associated Lysosphingolipids Inhibit NAD(P)H Oxidase-Dependent Monocyte Chemoattractant Protein-1 Production Arterioscler Thromb Vasc Biol, August 1, 2008; 28(8): 1542 - 1548. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Christoffersen, J. Ahnstrom, O. Axler, E. I. Christensen, B. Dahlback, and L. B. Nielsen The Signal Peptide Anchors Apolipoprotein M in Plasma Lipoproteins and Prevents Rapid Clearance of Apolipoprotein M from Plasma J. Biol. Chem., July 4, 2008; 283(27): 18765 - 18772. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. M. deGoma, R. L. deGoma, and D. J. Rader Beyond high-density lipoprotein cholesterol levels evaluating high-density lipoprotein function as influenced by novel therapeutic approaches. J. Am. Coll. Cardiol., June 10, 2008; 51(23): 2199 - 2211. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Carnemolla, X. Ren, T. K. Biswas, S. C. Meredith, C. A. Reardon, J. Wang, and G. S. Getz The Specific Amino Acid Sequence between Helices 7 and 8 Influences the Binding Specificity of Human Apolipoprotein A-I for High Density Lipoprotein (HDL) Subclasses: A POTENTIAL FOR HDL PREFERENTIAL GENERATION J. Biol. Chem., June 6, 2008; 283(23): 15779 - 15788. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. T. Bloedon, R. Dunbar, D. Duffy, P. Pinell-Salles, R. Norris, B. J. DeGroot, R. Movva, M. Navab, A. M. Fogelman, and D. J. Rader Safety, pharmacokinetics, and pharmacodynamics of oral apoA-I mimetic peptide D-4F in high-risk cardiovascular patients J. Lipid Res., June 1, 2008; 49(6): 1344 - 1352. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D J Hausenloy and D M Yellon Targeting residual cardiovascular risk: raising high-density lipoprotein cholesterol levels Heart, June 1, 2008; 94(6): 706 - 714. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Depke, G. Fusch, G. Domanska, R. Geffers, U. Volker, C. Schuett, and C. Kiank Hypermetabolic Syndrome as a Consequence of Repeated Psychological Stress in Mice Endocrinology, June 1, 2008; 149(6): 2714 - 2723. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Movva and D. J. Rader Laboratory Assessment of HDL Heterogeneity and Function Clin. Chem., May 1, 2008; 54(5): 788 - 800. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Araujo, B. Barajas, M. Kleinman, X. Wang, B. J. Bennett, K. W. Gong, M. Navab, J. Harkema, C. Sioutas, A. J. Lusis, et al. Ambient Particulate Pollutants in the Ultrafine Range Promote Early Atherosclerosis and Systemic Oxidative Stress Circ. Res., March 14, 2008; 102(5): 589 - 596. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Valiyaveettil, N. Kar, M. Z. Ashraf, T. V. Byzova, M. Febbraio, and E. A. Podrez Oxidized high-density lipoprotein inhibits platelet activation and aggregation via scavenger receptor BI Blood, February 15, 2008; 111(4): 1962 - 1971. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Genest The Yin and Yang of high-density lipoprotein cholesterol. J. Am. Coll. Cardiol., February 12, 2008; 51(6): 643 - 644. [Full Text] [PDF]
|
|
|
|
|
|
M. Moerland, H. Samyn, T. van Gent, M. Jauhiainen, J. Metso, R. van Haperen, F. Grosveld, A. van Tol, and R. de Crom Atherogenic, enlarged, and dysfunctional HDL in human PLTP/apoA-I double transgenic mice J. Lipid Res., December 1, 2007; 48(12): 2622 - 2631. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. I. van Leuven, R. Hezemans, J. H. Levels, S. Snoek, P. C. Stokkers, G. K. Hovingh, J. J. P. Kastelein, E. S. Stroes, E. de Groot, and D. W. Hommes Enhanced atherogenesis and altered high density lipoprotein in patients with Crohn's disease J. Lipid Res., December 1, 2007; 48(12): 2640 - 2646. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Grenier, F. S. Maupas, J.-F. Beaulieu, E. Seidman, E. Delvin, A. Sane, E. Tremblay, C. Garofalo, and E. Levy Effect of retinoic acid on cell proliferation and differentiation as well as on lipid synthesis, lipoprotein secretion, and apolipoprotein biogenesis Am J Physiol Gastrointest Liver Physiol, December 1, 2007; 293(6): G1178 - G1189. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. C. Newman, H. Bang, S. I. Hussain, and J. F. Toole Association of diabetes, homocysteine, and HDL with cognition and disability after stroke Neurology, November 27, 2007; 69(22): 2054 - 2062. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Van Eck, M. Hoekstra, R. B. Hildebrand, Y. Yaong, D. Stengel, J. K. Kruijt, W. Sattler, U. J.F. Tietge, E. Ninio, T. J.C. Van Berkel, et al. Increased Oxidative Stress in Scavenger Receptor BI Knockout Mice With Dysfunctional HDL Arterioscler Thromb Vasc Biol, November 1, 2007; 27(11): 2413 - 2419. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Terasaka, N. Wang, L. Yvan-Charvet, and A. R. Tall High-density lipoprotein protects macrophages from oxidized low-density lipoprotein-induced apoptosis by promoting efflux of 7-ketocholesterol via ABCG1 PNAS, September 18, 2007; 104(38): 15093 - 15098. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Parastatidis, L. Thomson, D. M. Fries, R. E. Moore, J. Tohyama, X. Fu, S. L. Hazen, H. F.G. Heijnen, M. K. Dennehy, D. C. Liebler, et al. Increased Protein Nitration Burden in the Atherosclerotic Lesions and Plasma of Apolipoprotein A-I Deficient Mice Circ. Res., August 17, 2007; 101(4): 368 - 376. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. S. Davidson and T. B. Thompson The Structure of Apolipoprotein A-I in High Density Lipoproteins J. Biol. Chem., August 3, 2007; 282(31): 22249 - 22253. [Full Text] [PDF]
|
|
|
|
 |
|
 A. Isaacs, Y. S. Aulchenko, A. Hofman, E. J. G. Sijbrands, F. A. Sayed-Tabatabaei, O. H. Klungel, A.-H. Maitland-van der Zee, B. H. Ch. Stricker, B. A. Oostra, J. C. M. Witteman, et al. Epistatic Effect of Cholesteryl Ester Transfer Protein and Hepatic Lipase on Serum High-Density Lipoprotein Cholesterol Levels J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2680 - 2687. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J Hamilton, G. T Chew, and G. F Watts Therapeutic regulation of endothelial dysfunction in type 2 diabetes mellitus Diabetes and Vascular Disease Research, June 1, 2007; 4(2): 89 - 102. [Abstract] [PDF]
|
|
|
|
|
|
L. A. Morehouse, E. D. Sugarman, P.-A. Bourassa, T. M. Sand, F. Zimetti, F. Gao, G. H. Rothblat, and A. J. Milici Inhibition of CETP activity by torcetrapib reduces susceptibility to diet-induced atherosclerosis in New Zealand White rabbits J. Lipid Res., June 1, 2007; 48(6): 1263 - 1272. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. M. Gharavi, P. S. Gargalovic, I. Chang, J. A. Araujo, M. J. Clark, W. L. Szeto, A. D. Watson, A. J. Lusis, and J. A. Berliner High-Density Lipoprotein Modulates Oxidized Phospholipid Signaling in Human Endothelial Cells From Proinflammatory to Anti-inflammatory Arterioscler Thromb Vasc Biol, June 1, 2007; 27(6): 1346 - 1353. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. S. Birjmohun, S. I. van Leuven, J. H.M. Levels, C. van 't Veer, J. A. Kuivenhoven, J. C.M. Meijers, M. Levi, J. J.P. Kastelein, T. van der Poll, and E. S.G. Stroes High-Density Lipoprotein Attenuates Inflammation and Coagulation Response on Endotoxin Challenge in Humans Arterioscler Thromb Vasc Biol, May 1, 2007; 27(5): 1153 - 1158. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Sarov-Blat, R. S. Kiss, B. Haidar, N. Kavaslar, M. Jaye, M. Bertiaux, K. Steplewski, M. R. Hurle, D. Sprecher, R. McPherson, et al. Predominance of a Proinflammatory Phenotype in Monocyte-Derived Macrophages From Subjects With Low Plasma HDL-Cholesterol Arterioscler Thromb Vasc Biol, May 1, 2007; 27(5): 1115 - 1122. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. J.P. Kastelein, S. I. van Leuven, L. Burgess, G. W. Evans, J. A. Kuivenhoven, P. J. Barter, J. H. Revkin, D. E. Grobbee, W. A. Riley, C. L. Shear, et al. Effect of Torcetrapib on Carotid Atherosclerosis in Familial Hypercholesterolemia N. Engl. J. Med., April 19, 2007; 356(16): 1620 - 1630. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Sumi, M. Sata, S.-i. Miura, K.-A. Rye, N. Toya, Y. Kanaoka, K. Yanaga, T. Ohki, K. Saku, and R. Nagai Reconstituted High-Density Lipoprotein Stimulates Differentiation of Endothelial Progenitor Cells and Enhances Ischemia-Induced Angiogenesis Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 813 - 818. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. R. Tall CETP Inhibitors to Increase HDL Cholesterol Levels N. Engl. J. Med., March 29, 2007; 356(13): 1364 - 1366. [Full Text] [PDF]
|
|
|
|
|
|
S. Eichinger, N. M. Pecheniuk, G. Hron, H. Deguchi, M. Schemper, P. A. Kyrle, and J. H. Griffin High-Density Lipoprotein and the Risk of Recurrent Venous Thromboembolism Circulation, March 27, 2007; 115(12): 1609 - 1614. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Van Eck, D. Ye, R. B. Hildebrand, J. Kar Kruijt, W. de Haan, M. Hoekstra, P. C.N. Rensen, C. Ehnholm, M. Jauhiainen, and T. J.C. Van Berkel Important Role for Bone Marrow-Derived Cholesteryl Ester Transfer Protein in Lipoprotein Cholesterol Redistribution and Atherosclerotic Lesion Development in LDL Receptor Knockout Mice Circ. Res., March 16, 2007; 100(5): 678 - 685. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Nicholls, E. M. Tuzcu, I. Sipahi, A. W. Grasso, P. Schoenhagen, T. Hu, K. Wolski, T. Crowe, M. Y. Desai, S. L. Hazen, et al. Statins, High-Density Lipoprotein Cholesterol, and Regression of Coronary Atherosclerosis JAMA, February 7, 2007; 297(5): 499 - 508. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. K. Shah Inhibition of CETP as a novel therapeutic strategy for reducing the risk of atherosclerotic disease Eur. Heart J., January 1, 2007; 28(1): 5 - 12. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Kimura, H. Tomura, C. Mogi, A. Kuwabara, A. Damirin, T. Ishizuka, A. Sekiguchi, M. Ishiwara, D.-S. Im, K. Sato, et al. Role of Scavenger Receptor Class B Type I and Sphingosine 1-Phosphate Receptors in High Density Lipoprotein-induced Inhibition of Adhesion Molecule Expression in Endothelial Cells J. Biol. Chem., December 8, 2006; 281(49): 37457 - 37467. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M McMahon, J Grossman, W Chen, and B H Hahn Inflammation and the pathogenesis of atherosclerosis in systemic lupus erythematosus Lupus, November 1, 2006; 15(11_suppl): 59 - 69. [Abstract] [PDF]
|
|
|
|
 |
|
 W. S. Kerwin, K. D. O'Brien, M. S. Ferguson, N. Polissar, T. S. Hatsukami, and C. Yuan Inflammation in Carotid Atherosclerotic Plaque: A Dynamic Contrast-enhanced MR Imaging Study Radiology, November 1, 2006; 241(2): 459 - 468. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Libby and P. M. Ridker Inflammation and Atherothrombosis: From Population Biology and Bench Research to Clinical Practice J. Am. Coll. Cardiol., October 27, 2006; 48(9_Suppl_A): A33 - A46. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. A. Thompson and R. L. Kitchens Native High-Density Lipoprotein Augments Monocyte Responses to Lipopolysaccharide (LPS) by Suppressing the Inhibitory Activity of LPS-Binding Protein J. Immunol., October 1, 2006; 177(7): 4880 - 4887. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Tschoepe and B. Stratmann Plaque stability and plaque regression: new insights Eur. Heart J. Suppl., October 1, 2006; 8(suppl_F): F34 - F39. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Barter Options for therapeutic intervention: how effective are the different agents? Eur. Heart J. Suppl., October 1, 2006; 8(suppl_F): F47 - F53. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Ranalletta, N. Wang, S. Han, L. Yvan-Charvet, C. Welch, and A. R. Tall Decreased Atherosclerosis in Low-Density Lipoprotein Receptor Knockout Mice Transplanted With Abcg1-/- Bone Marrow Arterioscler Thromb Vasc Biol, October 1, 2006; 26(10): 2308 - 2315. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Theilmeier, C. Schmidt, J. Herrmann, P. Keul, M. Schafers, I. Herrgott, J. Mersmann, J. Larmann, S. Hermann, J. Stypmann, et al. High-Density Lipoproteins and Their Constituent, Sphingosine-1-Phosphate, Directly Protect the Heart Against Ischemia/Reperfusion Injury In Vivo via the S1P3 Lysophospholipid Receptor Circulation, September 26, 2006; 114(13): 1403 - 1409. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. J. Barter and K.-A. Rye Homocysteine and Cardiovascular Disease: Is HDL the Link? Circ. Res., September 15, 2006; 99(6): 565 - 566. [Full Text] [PDF]
|
|
|
|
|
|
C. Shah, R. Hari-Dass, and J. G. Raynes Serum amyloid A is an innate immune opsonin for Gram-negative bacteria Blood, September 1, 2006; 108(5): 1751 - 1757. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Mineo, H. Deguchi, J. H. Griffin, and P. W. Shaul Endothelial and Antithrombotic Actions of HDL Circ. Res., June 9, 2006; 98(11): 1352 - 1364. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. de Haan, P. K. Witting, N. Stefanovic, J. Pete, M. Daskalakis, I. Kola, R. Stocker, and J. J. Smolich Lack of the antioxidant glutathione peroxidase-1 does not increase atherosclerosis in C57BL/J6 mice fed a high-fat diet J. Lipid Res., June 1, 2006; 47(6): 1157 - 1167. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. C.N. Rensen and L. M. Havekes Cholesteryl Ester Transfer Protein Inhibition: Effect on Reverse Cholesterol Transport? Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 681 - 684. [Full Text] [PDF]
|
|
|
|
 |
|
 I. O. Ottestad, B. Halvorsen, T. R. Balstad, K. Otterdal, G. I. Borge, F. Brosstad, A. M. Myhre, L. Ose, M. S. Nenseter, and K. B. Holven Triglyceride-Rich HDL3 from Patients with Familial Hypercholesterolemia Are Less Able to Inhibit Cytokine Release or to Promote Cholesterol Efflux J. Nutr., April 1, 2006; 136(4): 877 - 881. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. H.E.M. Klerkx, K. E. Harchaoui, W. A. van der Steeg, S. M. Boekholdt, E. S.G. Stroes, J. J.P. Kastelein, and J. A. Kuivenhoven Cholesteryl Ester Transfer Protein (CETP) Inhibition Beyond Raising High-Density Lipoprotein Cholesterol Levels: Pathways by Which Modulation of CETP Activity May Alter Atherogenesis Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 706 - 715. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Van Eck, R. R. Singaraja, D. Ye, R. B. Hildebrand, E. R. James, M. R. Hayden, and T. J.C. Van Berkel Macrophage ATP-Binding Cassette Transporter A1 Overexpression Inhibits Atherosclerotic Lesion Progression in Low-Density Lipoprotein Receptor Knockout Mice Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 929 - 934. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Ji, G. F. Watts, A. G. Johnson, D. C. Chan, E. M. M. Ooi, K.-A. Rye, A. P. Serone, and P. H. R. Barrett High-Density Lipoprotein (HDL) Transport in the Metabolic Syndrome: Application of a New Model for HDL Particle Kinetics J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 973 - 979. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. A. Ajees, G. M. Anantharamaiah, V. K. Mishra, M. M. Hussain, and H. M. K. Murthy Crystal structure of human apolipoprotein A-I: Insights into its protective effect against cardiovascular diseases PNAS, February 14, 2006; 103(7): 2126 - 2131. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Kawakami, M. Aikawa, P. Libby, P. Alcaide, F. W. Luscinskas, and F. M. Sacks Apolipoprotein CIII in Apolipoprotein B Lipoproteins Enhances the Adhesion of Human Monocytic Cells to Endothelial Cells Circulation, February 7, 2006; 113(5): 691 - 700. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Armanini, C. Fiore, L. A Calo, S. Takai, and M. Miyazaki Mononuclear Leukocyte Mineralocorticoid Receptors * Response Hypertension, February 1, 2006; 47(2): e4 - e5. [Full Text] [PDF]
|
|
|
|
|
|
D. Seetharam, C. Mineo, A. K. Gormley, L. L. Gibson, W. Vongpatanasin, K. L. Chambliss, L. D. Hahner, M. L. Cummings, R. L. Kitchens, Y. L. Marcel, et al. High-Density Lipoprotein Promotes Endothelial Cell Migration and Reendothelialization via Scavenger Receptor-B Type I Circ. Res., January 6, 2006; 98(1): 63 - 72. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Navab, G.M. Anantharamaiah, and A. M. Fogelman An Apolipoprotein A-I Mimetic Works Best in the Presence of Apolipoprotein A-I Circ. Res., November 25, 2005; 97(11): 1085 - 1086. [Full Text] [PDF]
|
|
|
|
|
|
S. J. Nicholls, B. Cutri, S. G. Worthley, P. Kee, K.-A. Rye, S. Bao, and P. J. Barter Impact of Short-Term Administration of High-Density Lipoproteins and Atorvastatin on Atherosclerosis in Rabbits Arterioscler Thromb Vasc Biol, November 1, 2005; 25(11): 2416 - 2421. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. E. Moore, M. Navab, J. S. Millar, F. Zimetti, S. Hama, G. H. Rothblat, and D. J. Rader Increased Atherosclerosis in Mice Lacking Apolipoprotein A-I Attributable to Both Impaired Reverse Cholesterol Transport and Increased Inflammation Circ. Res., October 14, 2005; 97(8): 763 - 771. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Fuster, P. R. Moreno, Z. A. Fayad, R. Corti, and J. J. Badimon Atherothrombosis and High-Risk Plaque: Part I: Evolving Concepts J. Am. Coll. Cardiol., September 20, 2005; 46(6): 937 - 954. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P.J. Barter Cardioprotective Effects of High-Density Lipoproteins: The Evidence Strengthens Arterioscler Thromb Vasc Biol, July 1, 2005; 25(7): 1305 - 1306. [Full Text] [PDF]
|
|
|
|
|
|
M. Navab, G.M. Anantharamaiah, S. Hama, G. Hough, S. T. Reddy, J. S. Frank, D. W. Garber, S. Handattu, and A. M. Fogelman D-4F and Statins Synergize to Render HDL Antiinflammatory in Mice and Monkeys and Cause Lesion Regression in Old Apolipoprotein E-Null Mice Arterioscler Thromb Vasc Biol, July 1, 2005; 25(7): 1426 - 1432. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Shepherd Raising HDL-cholesterol and lowering CHD risk: does intervention work? Eur. Heart J. Suppl., July 1, 2005; 7(suppl_F): F15 - F22. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Chait, C. Y. Han, J. F. Oram, and J. W. Heinecke Thematic review series: The Immune System and Atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease? J. Lipid Res., March 1, 2005; 46(3): 389 - 403. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||