© 2000 American Heart Association, Inc.
MiniReviews |
NAD(P)H Oxidase
Role in Cardiovascular Biology and Disease
From the Department of Medicine, Division of Cardiology, Emory University, Atlanta, Ga.
Correspondence to Kathy K. Griendling, Division of Cardiology, Emory University School of Medicine, 1639 Pierce Dr, 319 WMB, Atlanta, GA 30322. E-mail kgriend{at}emory.edu
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Abstract |
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 Top Abstract IntroductionNAD(P)H OxidaseBiological Effects of NAD(P)H...Future DirectionsReferences |
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Abstract—Reactive oxygen species have emerged as important molecules in cardiovascular function. Recent work has shown that NAD(P)H oxidases are major sources of superoxide in vascular cells and myocytes. The biochemical characterization, activation paradigms, structure, and function of this enzyme are now partly understood. Vascular NAD(P)H oxidases share some, but not all, characteristics of the neutrophil enzyme. In response to growth factors and cytokines, they produce superoxide, which is metabolized to hydrogen peroxide, and both of these reactive oxygen species serve as second messengers to activate multiple intracellular signaling pathways. The vascular NAD(P)H oxidases have been found to be essential in the physiological response of vascular cells, including growth, migration, and modification of the extracellular matrix. They have also been linked to hypertension and to pathological states associated with uncontrolled growth and inflammation, such as atherosclerosis.
Key Words: NAD(P)H oxidase • reactive oxygen species • superoxide • vascular cells
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Introduction |
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TopAbstractIntroductionNAD(P)H OxidaseBiological Effects of NAD(P)H...Future DirectionsReferences |
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Recent work has provided a broad experimental base supporting a critical role for oxidative stress in the normal functioning of cardiac and vascular cells, as well as in the pathogenesis of vascular disease. The concept of oxidation of LDL as an initiating event in vascular lesion formation has been extended to encompass numerous other roles for oxidation-reduction reactions in cardiovascular biology. An emerging common theme of these studies is that an NAD(P)H oxidase is a major source of superoxide in vascular cells and myocytes. A plethora of experimental data has recently been generated concerning the mechanisms of activation of this enzyme, its role in normal cell functioning, and its participation in cardiovascular disease.
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NAD(P)H Oxidase |
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TopAbstractIntroductionNAD(P)H OxidaseBiological Effects of NAD(P)H...Future DirectionsReferences |
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It has been known for years that vascular and cardiac tissues are rich sources of reactive oxygen species (ROS), including superoxide (O2·-), hydrogen peroxide (H2O2), and nitric oxide (NO·). Virtually every cell type in the vascular wall has been shown to produce and be regulated by ROS (for review see References 1 and 2 ). Early work identified xanthine oxidase as a prime source of endothelium-dependent O2·- production.3 4 It has subsequently been established that smooth muscle cells and fibroblasts account for the majority of O2·- produced in the normal vessel wall.5 6 7 8 Currently, attention is focused on NAD(P)H oxidases as critical determinants of the redox state of blood vessels and the myocardium.
Biochemical Characteristics
The NAD(P)H oxidases of the cardiovascular system
are membrane-associated enzymes that catalyze the 1-electron reduction
of oxygen using NADH or NADPH as the electron donor.
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10 µmol/L.
Recent work suggests that this substrate preference may depend somewhat
on the method of detection. Superoxide production in
nonphagocytic cells is often measured using lucigenin, an acridylium
dinitrite compound that emits light on reduction and interaction with
O2·-.16
Lucigenin has been criticized because of its ability to undergo redox
cycling, in particular when NADH is used as a substrate.17
Low levels of lucigenin (<10 µmol/L) do not suffer from this
drawback,17 and under these conditions, NADPH appears to
be the major substrate of the vascular enzymes (D. Sorescu, K.K.
Griendling, unpublished observations, 1999). Analysis
with electron spin resonance spectroscopy using the spin trap
5-diethoxyphosphoryl-5-methyl-pyrroline-N-oxide (DEPMPO)
indicates that NADPH and NADH are equally good substrates in VSMCs (D.
Sorescu, K.K. Griendling, unpublished observations, 1999) but that
NADH-driven O2·-
production predominates in endothelial cells
(ECs) (D. Harrison, personal communication, June 1999). Further
investigation into the substrates utilized by these enzymes under
different physiological conditions is
imperative. Vascular NAD(P)H oxidase activity has been better studied than the activity of the cardiac enzyme. These enzymes appear to reside in cell membranes. We and others have observed NADH- or NADPH-driven O2·- production in the 100 000-g membrane fraction, suggesting a plasma membrane or microsomal localization.8 9 18 19 There is some controversy regarding the orientation of these enzymes. By analogy with the neutrophil enzyme (see below), the oxidase should span the membrane, utilizing intracellular NADH or NADPH and transferring electrons across the membrane to extracellular oxygen. In support of this concept, O2·- release has been observed from ECs and fibroblasts.18 20 However, in VSMCs, O2·- and H2O2 production appears to be mainly intracellular,6 21 and in fibroblasts, an NADH-driven ectoenzyme has been identified.22 It has also been shown that addition of NADPH or NADH extracellularly augments O2·- formation,23 calling into question whether nonphagocytic cells exhibit the classical inside-out orientation of neutrophils.
The cardiovascular NAD(P)H oxidases are low-output, slow-release enzymes of which the biochemical characteristics differ considerably from those of the neutrophil NADPH oxidase. Estimates of O2·- production in vascular cells suggest that the capacity of these enzymes is about one third that of the neutrophil.24 Furthermore, the vascular enzymes appear to have a moderate constitutive activity that is absent in phagocytes.7 The kinetics of activation on cellular stimulation are also unique; O2·- is produced in minutes to hours in ECs, VSMCs, and fibroblasts,6 25 26 in contrast to the almost instantaneous release seen in neutrophils. Despite these differences, the neutrophil and vascular enzymes share some characteristics; both are inhibited by diphenylene iodonium (DPI), an inhibitor of flavin-containing oxidases, and both are stimulated by agonists and arachidonic acid.24
Structure
The above comparison suggests that although the
cardiovascular oxidases are similar to the neutrophil
NADPH oxidase, they represent a unique family of enzymes
(Figure 1
). The neutrophil oxidase
consists of 4 major subunits: a plasma membrane spanning cytochrome
b558 composed of a large subunit gp91phox and a smaller, p22phox
subunit and 2 cytosolic components p47phox and p67phox. The low
molecular weight G protein rac2 (in some cells rac1) participates in
assembly of the active complex, and a second G protein, rap1A,
copurifies with the enzyme and may participate in
deactivation.27 Much effort has been directed at
identifying which of these subunits are present in
cardiovascular cells and in determining whether a
similar multimeric complex might be responsible for oxidase
activity (Table). Using molecular
biological approaches, mRNAs for gp91phox, p22phox, p47phox, and
p67phox have been demonstrated in ECs14 28 and adventitial
cells.7 VSMCs and mesangial cells appear to
express p22phox, p47phox, and rac1, but not
gp91phox,19 29 30 with the possible exception of
pulmonary artery smooth muscle, in which gp91phox has been
detected.31 p67phox has been found in
mesangial cells29 but has been reported to be
absent in VSMCs.19 The phox content of fibroblasts is
controversial; in some cases, all subunits have been
detected,7 whereas in others, only p22phox, p47phox, and
p67phox were identified.32 33
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Proving a role for each of these components in oxidase activity has been challenging. Several years ago, we showed that antisense p22phox stably transfected into cultured VSMCs resulted in a 50% decrease in angiotensin II–stimulated NAD(P)H oxidase activity.30 Patterson et al19 reported a good correlation between thrombin-induced O2·- production and translocation and expression of p47phox and rac2, providing indirect evidence that these 2 subunits participate in the active enzymatic complex. Using negative dominant rac1, Irani et al34 demonstrated that O2·- production in fibroblasts was dependent on functional rac1. Similarly, Pagano et al7 recently suggested that p67phox was required for fibroblast NAD(P)H oxidase activity by showing that immunodepletion of p67phox resulted in a decrease in O2·- production. In ECs, phox components are poorly detected at the protein level, and cytochrome b558 is not measurable spectrophotometrically,14 so that functional evidence in this cell type is lacking. The ability of DPI to inhibit EC O2·- production, however, suggests that a similar enzyme complex may be responsible.
Despite these advances, it remains to be determined in each of these cells which subunits form functional complexes and whether as-yet-unidentified proteins participate in O2·- formation. If cardiovascular cells contain a neutrophil-like functional oxidase, it is essential to demonstrate the existence of the electron transport moiety of the protein. In neutrophils, it has been suggested that the 2 components of cytochrome b558, gp91phox and p22phox, stabilize each other.35 The finding that some nonphagocytic cells express p22phox in the absence of gp91phox raises the possibility that there are gp91phox isoforms that serve a similar function in these cells. One of the first indications that this might be the case came from a seminal observation by Meier et al33 that O2·- production was normal in fibroblasts from a chronic granulomatous disease patient whose neutrophil oxidase functioned at only 10% normal capacity. They further showed that the fibroblast cytochrome was immunologically distinct from that of phagocytes. Recently, a homologue of gp91phox (termed mox-1, for mitogenic oxidase) was cloned from human colon carcinoma and rat aortic smooth muscle cells.36 Human mox1 has 56% identity with human gp91phox, and importantly, all of the major functional domains (pyridine binding sites, flavin nucleotide binding sites, and potential heme binding sites) are completely conserved. Furthermore, the hydrophobic profiles of mox1 and gp91phox are nearly identical, suggesting similar cellular localization. Overexpression of mox1 in fibroblasts leads to an increase in O2·- production and a transformation in phenotype to increased, anchorage-independent cell growth. Moreover, expression of mox1 antisense in VSMCs results in a decrease in serum-stimulated NADPH-driven O2·- production and a decrease in cell growth. Fragments of other gp91phox homologues have been identified,36 but their functional role remains to be established. The discovery of mox1 indicates that it is likely that the vascular NAD(P)H oxidases belong to a novel family of growth factor–responsive oxidative enzymes.
Mechanism of Activation
One of the most important attributes of the
cardiovascular oxidase is its responsiveness to
hormones, hemodynamic forces, and local
metabolic changes. It has been clearly demonstrated that
the activity of the vascular oxidase is increased by the important
vasoactive agonist angiotensin II. Angiotensin
II increases NADH- and NADPH-driven
O2·- production in
cultured VSMCs6 and aortic adventitial
fibroblasts25 and increases DPI-inhibitable ROS
production in mesangial cells.37
Thrombin, platelet-derived growth factor (PDGF), tumor necrosis
factor-
(TNF-), and lactosylceramide also stimulate NAD(P)H
oxidase-dependent O2·- in
VSMCs.15 19 38 39 40 With regard to metabolic
changes, reoxygenation and the accompanying increase in
lactate stimulate NADH oxidase activity in cardiac
myocytes.11 Fibroblasts exhibit increased NADH- or
NADPH-dependent O2·-
production in response to TNF-, interleukin-1, and
platelet-activating factor.41 42 Moreover,
transforming growth factor-ß1 causes a slow, sustained
H2O2 release that is
inhibitable by DPI, but it has no effect on
O2·- production,
raising the possibility that the NAD(P)H oxidase might directly
participate in the 2-electron reduction of oxygen to
H2O2.43 In
ECs, mechanical forces stimulate NAD(P)H oxidase
activity,44 45 but agonist responsiveness remains to be
established. Both unidirectional and oscillatory shear stresses
increase O2·-
production. Exposure of cultured human umbilical vein ECs to 5
or 20 dyne/cm2 laminar shear stress results in a
transient elevation in O2·-
formation45 46 that is apparently derived from activation
of an NAD(P)H oxidase, whereas oscillatory shear causes a sustained (up
to 24 hours) increase in oxidase activity.45
Regulation of oxidase activity in cardiovascular
cells occurs at at least 2 levels. First, activation of the oxidase can
be mediated by intracellular second messengers, including
calcium.42 Although neutrophil oxidase activity is
regulated by protein kinase C,47 it is unclear whether
this kinase participates in activation of nonphagocytic oxidases.
Phorbol 12-myristate 13-acetate, a protein kinase C
activator, has no effect on adventitial
O2·-
production,7 but it increases NAD(P)H oxidase
activity in VSMCs (D. Sorescu, K.K. Griendling, unpublished
observations, 1999). It has recently been shown that
lipoxygenase metabolites of arachidonic
acid mediate angiotensin II stimulation of the NAD(P)H
oxidase in VSMCs,48 but the upstream signaling pathways
remain to be defined. Secondly, oxidase activity can also be modulated
by upregulation of the component mRNAs. For example, TNF- increases
NAD(P)H oxidase activity in VSMCs over 24 hours, an event that is
dependent on increased transcription of p22phox.15 p22phox
mRNA and O2·-
production are upregulated in the aortas of rats made
hypertensive by angiotensin II infusion,49 and
angiotensin II increases the expression of p67phox in
adventitial fibroblasts.25 Conversely, Marumo et
al50 showed that dexamethasone inhibited
PDGF-stimulated O2·- and
H2O2 production and
decreased p22phox mRNA expression in VSMCs but not in neutrophils.
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Biological Effects of NAD(P)H Oxidase Activation |
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TopAbstractIntroductionNAD(P)H OxidaseBiological Effects of NAD(P)H...Future DirectionsReferences |
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ROS and NAD(P)H oxidases have been implicated in numerous cellular processes and vascular diseases (Figure 2
). These enzymes have been
proposed to be oxygen sensors and to participate in hypoxic
vasoconstriction12 and/or vasodilation,51 but
this has recently been called into question by Archer et
al,31 who showed that oxygen sensing was normal in
gp91phox-deficient mice. The discovery of gp91phox homologues may help
to settle this controversy. Production of
O2·- in the vessel wall has
been shown to inactivate nitric oxide, leading to the
production of peroxynitrite and impaired
endothelium-dependent vasodilation52 53 ;
oxidize LDL54 ; increase adhesion molecule expression in
ECs resulting in monocyte infiltration55 ; and
activate matrix metalloproteinases, leading to vascular
remodeling.56 NAD(P)H oxidase-derived
O2·- and
H2O2 are intimately
involved in the growth response of VSMCs and
fibroblasts6 21 30 34 39 and also participate in VSMC
migration39 and, in some cases, cellular
apoptosis.57 These ROS are thus functioning as
signaling molecules to mediate specific cellular responses.
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NAD(P)H-Derived ROS as Second Messengers
Stimulation of cell surface receptors with growth factors or
agonists activates various cellular signaling pathways,
including protein tyrosine kinases, serine/threonine kinases,
phospholipases, and Ca2+-dependent pathways.
Importantly, exogenous application of ROS stimulates many of these same
cascades. Ligand-induced receptor activation rapidly increases
intracellular O2·- and
H2O2, and accumulating
evidence suggests that these endogenously derived ROS play
critical roles as intracellular signaling molecules. The molecular
targets of ROS in agonist-stimulated signal transduction have been the
subject of intense recent investigation.
The mitogen-activated protein kinase (MAPK) family comprises key regulatory proteins that control the cellular response to growth, apoptosis, and stress signals. In VSMCs, although both H2O2 and O2·- promote cell growth, only O2·- activates p42/44 MAPKs (extracellular signal–regulated kinase [ERK] 1 and ERK2).58 Interestingly, angiotensin II, which produces both O2·- and H2O2, potently activates ERK1/ERK2 and p38 MAPK.59 60 However, only p38 MAPK activation by angiotensin II is sensitive to both inhibition of NAD(P)H oxidase activity and catalase overexpression in VSMCs.60 In contrast, PDGF-induced ERK1/ERK2 activation is inhibited by exogenously applied catalase.39 ERK1/ERK2 activation in ECs can also be redox sensitive, as shown by the observation that shear stress–induced ERK1/ERK2 tyrosine phosphorylation is inhibited by antioxidants and negative dominant rac-1.61 Finally, in perfused rat hearts, JNK and p38 MAPK are activated by H2O2 and ischemia reperfusion.62
The cell survival kinase Akt (protein kinase B) is another potential redox-sensitive kinase.63 Both exogenous H2O2 and angiotensin II induce Akt activation in VSMCs.64 Importantly, angiotensin II–induced Akt phosphorylation is inhibited by DPI or overexpression of catalase, indicating a role for the NAD(P)H oxidase in agonist-induced Akt activation. Akt may be involved in the redox-sensitive signaling leading to VSMC hypertrophy, because dominant negative Akt inhibits angiotensin II–stimulated [3H]leucine incorporation in cultured VSMCs.64
Other potential redox-sensitive signaling targets include ras/rac,34 65 66 67 c-src,68 protein kinase C,69 tyrosine phosphatases,70 71 72 and regulation of Ca2+ signaling (reviewed in References 2 and 73 ). Our recent data suggest that not only are the proteins themselves potential targets, but also interactions between molecules within a signaling complex may be modified by ROS (M. Ushio-Fukai, unpublished data, 1999).
Redox-Sensitive Gene Expression
Because of the manifold hormones and growth factors that
alter tissue and intracellular levels of ROS and the varied and
critical signaling pathways activated by ROS, it is not
surprising that many cardiovascular-related genes are
redox sensitive. ROS regulate several general classes of genes,
including adhesion molecules and chemotactic factors, antioxidant
enzymes, and vasoactive substances. Some of these genes clearly
provide an adaptive response, such as the induction of
superoxide dismutase (SOD) and catalase by
H2O2.74 As
opposed to being responsive to externally applied oxidant stress or to
being regulated by an unknown source of ROS, only a few of these genes
have been demonstrated to be downstream of the NAD(P)H oxidases. Arai
et al75 showed that induction of intercellular adhesion
molecule-1 by TNF- was inhibited by multiple antioxidants, including
DPI. DPI also blocked lactosylceramide upregulation of intercellular
adhesion molecule-1.40 MCP-1 is another gene that appears
to be responsive to NAD(P)H oxidase activation. Oxidase
inhibitors attenuate the induction of MCP-1 by
angiotensin II76 and PDGF38 in
VSMCs, as well as by TNF- in fibroblasts. In contrast, stimulation
of MCP-1 by interleukin-1ß38 or by
TNF-77 in VSMCs is unaffected by antioxidants,
suggesting that redox-sensitive control of gene expression is both
tissue and stimulus specific.
NAD(P)H Oxidase and Cell Growth
One of the most important functions of NAD(P)H
oxidase–derived O2·- and
H2O2 in VSMCs and cardiac
myocytes is participation in cell growth. In VSMCs,
angiotensin II induces cellular hypertrophy by
acting through G protein–coupled AT1
receptors.78 79 It has recently been demonstrated that
angiotensin II–induced hypertrophy is mediated
by intracellularly produced
H2O2 that is derived, at
least in part, from a membrane-associated NAD(P)H
oxidase.6 21 30 This conclusion was based on 3 lines of
evidence. First, angiotensin II–induced
hypertrophy is abrogated by DPI, an inhibitor
of NAD(P)H oxidase.6 Second, reduction of NAD(P)H oxidase
activity by transfection of antisense p22phox inhibits both
H2O2 and
hypertrophy, suggesting that
H2O2 might be the relevant
ROS.30 This was confirmed by the third set of data, namely
that catalase overexpression attenuates the angiotensin
II–induced effects on growth.21 Similar results have been
found in cardiac myocytes, in which it was shown that
angiotensin II– and TNF-–induced
hypertrophy is associated with intracellular release of ROS
and that antioxidants blocked both events.80 Furthermore,
in VSMCs, endogenous ROS production is stimulated
by PDGF and epidermal growth factor,39 lactosylceramide (a
ceramide analogue present in atherosclerotic
plaque),81 phenylephrine,82 and
thrombin.19 In all cases, the increases in ROS and
proliferation induced by these agonists were shown to be inhibited by
antioxidants such as DPI, N-acetyl-cysteine, or
catalase.
NAD(P)H Oxidase and Atherosclerosis
The original hypothesis that atherosclerosis
is an inflammatory disease centered on oxidized LDL as the main
effector. It is clear, however, that oxidative stress plays a much
broader role in the pathogenesis of this disease. Animal models of
atherosclerosis have documented that all of the
constituents of the plaque produce and use
ROS.6 7 14 25 83 In cholesterol-fed rabbits,
O2·- is increased in the
aorta,26 and treatment with polyethyleneglycol SOD
reverses the impaired endothelial-dependent
relaxation.53
Recently, in a rabbit model of early atherosclerosis (Watanabe rabbits, in which hypercholesterolemia is secondary to a LDL-receptor defect), Warnholtz et al84 showed that vascular NADH-driven O2·- was increased 2-fold compared with control after 8 weeks. Endothelial denudation normalized the differences in O2·-, suggesting that the excess O2·- production was localized to the intima. Interestingly, treatment with the AT1 receptor antagonist BAY 10-6734 normalized O2·- and endothelial function and reduced early atherosclerotic lesion formation, suggesting a role for angiotensin II in this hypercholesterolemic model of early atherosclerosis.
In a chronic, advanced model of atherosclerosis (2 to 4 years of hypercholesterolemia), Miller et al85 found that aortas from Watanabe rabbits had O2·- levels 3 times higher than rabbits with normal levels of cholesterol. In contrast to the previous study, the correction of endothelial O2·- production with adenoviruses encoding Cu/Zn SOD or extracellular SOD did not improve endothelium-dependent relaxation.85 These data suggest that the cellular source and functional consequence of O2·- production may evolve in a spatiotemporal manner from the endothelium toward the medial-adventitial side of the vessel wall. This process bears a striking similarity to the spatiotemporal evolution of atherosclerosis.
In more advanced atherosclerotic lesions, VSMC NAD(P)H oxidase-derived
ROS may play a crucial role in progression and biological activity.
Angiotensin II, PDGF, and TNF- may increase ROS in the
atherosclerotic lesion by stimulating the local vascular myocytes to
produce ROS, as they do in culture. Subsequently, ROS may contribute to
LDL oxidation,54 local MCP-1
production,38 76 upregulation of adhesion
molecules and macrophage recruitment,55 75
endothelial dysfunction,53 and
extracellular matrix remodeling through collagen degradation and
eventually plaque rupture.56 86 87
NAD(P)H Oxidase and Hypertension
Compelling evidence has accumulated to support a role for
O2·- in various forms of
hypertension. In a spontaneously hypertensive rat model, Suzuki et
al88 showed that
O2·- is increased in venules
and arterioles, and Nakazono et al89 provided evidence
confirming the functional importance of ROS by demonstrating that
administration of heparin-binding SOD, which localizes within the
vessel wall, normalized the blood pressure of these rats. Rajagopalan
et al8 and Fukui et al90 demonstrated that
chronic infusion of angiotensin II in rats upregulates
vascular p22phox mRNA and increases NAD(P)H oxidase-derived
O2·-. Both the hypertension
and the increase in p22phox mRNA were prevented by pretreatment with
SOD.49 91 Hypertension was also correlated with high
oxidative stress in Dahl hypertensive rats.92 In contrast,
norepinephrine-induced hypertension increases neither
O2·- production nor
oxidase expression,8 suggesting that
O2·- is involved in only
certain forms of hypertension.
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Future Directions |
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TopAbstractIntroductionNAD(P)H OxidaseBiological Effects of NAD(P)H...Future DirectionsReferences |
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Although much progress has been made in identifying and characterizing the NAD(P)H oxidases, significant work remains. Further information concerning the molecular structure and activation mechanisms of the oxidase in different cardiovascular cells is needed. In addition, identification of the enzymatic and protein targets of oxidase-derived ROS should be a priority. The ultimate goal, of course, is the development of new therapeutic strategies for the treatment of the multitude of cardiovascular diseases of which the pathology derives in part or in total from increased oxidative stress. Understanding the molecular mechanisms leading to generation of ROS and the endogenous antioxidant enzymes responsible for their removal should provide new targets for the emerging therapeutic paradigm of gene therapy.
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Acknowledgments |
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This review was supported by NIH Grants HL38206, HL58000, and HL58863. We thank Carolyn Morris for excellent secretarial assistance.
This MiniReview is part of a thematic series on Oxidant Signaling in Cardiovascular Cells, which includes the following articles: NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease Crosstalk Between Nitric Oxide and Lipid Oxidation Systems: Implications for Vascular Disease Oxygen Radicals and Endothelial Dysfunction Oxidant Signaling in Vascular Cell Growth, Death, and Function Antioxidant Vitamins and Clinical Studies Vascular Oxygen Species Generation David G. Harrison, Guest Editor
Received September 2, 1999; accepted January 5, 2000.
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 H. A. Mostefai, F. Meziani, M. L. Mastronardi, A. Agouni, C. Heymes, C. Sargentini, P. Asfar, M. C. Martinez, and R. Andriantsitohaina Circulating Microparticles from Patients with Septic Shock Exert Protective Role in Vascular Function Am. J. Respir. Crit. Care Med., December 1, 2008; 178(11): 1148 - 1155. [Abstract] [Full Text] [PDF]
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 A. Szeto, D. A. Nation, A. J. Mendez, J. Dominguez-Bendala, L. G. Brooks, N. Schneiderman, and P. M. McCabe Oxytocin attenuates NADPH-dependent superoxide activity and IL-6 secretion in macrophages and vascular cells Am J Physiol Endocrinol Metab, December 1, 2008; 295(6): E1495 - E1501. [Abstract] [Full Text] [PDF]
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 S. Schmidt, T. H. Westhoff, P. Krauser, R. Ignatius, J. Jankowski, V. Jankowski, W. Zidek, and M. van der Giet The uraemic toxin phenylacetic acid impairs macrophage function Nephrol. Dial. Transplant., November 1, 2008; 23(11): 3485 - 3493. [Abstract] [Full Text] [PDF]
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C. D. Fike, J. C. Slaughter, M. R. Kaplowitz, Y. Zhang, and J. L. Aschner Reactive oxygen species from NADPH oxidase contribute to altered pulmonary vascular responses in piglets with chronic hypoxia-induced pulmonary hypertension Am J Physiol Lung Cell Mol Physiol, November 1, 2008; 295(5): L881 - L888. [Abstract] [Full Text] [PDF]
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E. Yamamoto, N. Tamamaki, T. Nakamura, K. Kataoka, Y. Tokutomi, Y.-F. Dong, M. Fukuda, S. Matsuba, H. Ogawa, and S. Kim-Mitsuyama Excess Salt Causes Cerebral Neuronal Apoptosis and Inflammation in Stroke-Prone Hypertensive Rats Through Angiotensin II-Induced NADPH Oxidase Activation Stroke, November 1, 2008; 39(11): 3049 - 3056. [Abstract] [Full Text] [PDF]
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D. Meng, D.-D. Lv, and J. Fang Insulin-like growth factor-I induces reactive oxygen species production and cell migration through Nox4 and Rac1 in vascular smooth muscle cells Cardiovasc Res, November 1, 2008; 80(2): 299 - 308. [Abstract] [Full Text] [PDF]
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Q. Sun, P. Yue, Z. Ying, A. J. Cardounel, R. D. Brook, R. Devlin, J.-S. Hwang, J. L. Zweier, L. C. Chen, and S. Rajagopalan Air Pollution Exposure Potentiates Hypertension Through Reactive Oxygen Species-Mediated Activation of Rho/ROCK Arterioscler Thromb Vasc Biol, October 1, 2008; 28(10): 1760 - 1766. [Abstract] [Full Text] [PDF]
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O. Handa, J. Stephen, and G. Cepinskas Role of endothelial nitric oxide synthase-derived nitric oxide in activation and dysfunction of cerebrovascular endothelial cells during early onsets of sepsis Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1712 - H1719. [Abstract] [Full Text] [PDF]
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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]
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T.-D. Liao, X.-P. Yang, Y.-H. Liu, E. G. Shesely, M. A. Cavasin, W. A. Kuziel, P. J. Pagano, and O. A. Carretero Role of Inflammation in the Development of Renal Damage and Dysfunction in Angiotensin II-Induced Hypertension Hypertension, August 1, 2008; 52(2): 256 - 263. [Abstract] [Full Text] [PDF]
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F. Tabet, E. L. Schiffrin, G. E. Callera, Y. He, G. Yao, A. Ostman, K. Kappert, N. K. Tonks, and R. M. Touyz Redox-Sensitive Signaling by Angiotensin II Involves Oxidative Inactivation and Blunted Phosphorylation of Protein Tyrosine Phosphatase SHP-2 in Vascular Smooth Muscle Cells From SHR Circ. Res., July 18, 2008; 103(2): 149 - 158. [Abstract] [Full Text] [PDF]
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N. Urao, H. Inomata, M. Razvi, H. W. Kim, K. Wary, R. McKinney, T. Fukai, and M. Ushio-Fukai Role of Nox2-Based NADPH Oxidase in Bone Marrow and Progenitor Cell Function Involved in Neovascularization Induced by Hindlimb Ischemia Circ. Res., July 18, 2008; 103(2): 212 - 220. [Abstract] [Full Text] [PDF]
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M. Al-Shabrawey, M. Rojas, T. Sanders, A. Behzadian, A. El-Remessy, M. Bartoli, A. K. Parpia, G. Liou, and R. B. Caldwell Role of NADPH Oxidase in Retinal Vascular Inflammation Invest. Ophthalmol. Vis. Sci., July 1, 2008; 49(7): 3239 - 3244. [Abstract] [Full Text] [PDF]
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M. J. Haurani, M. E. Cifuentes, A. D. Shepard, and P. J. Pagano Nox4 Oxidase Overexpression Specifically Decreases Endogenous Nox4 mRNA and Inhibits Angiotensin II-Induced Adventitial Myofibroblast Migration Hypertension, July 1, 2008; 52(1): 143 - 149. [Abstract] [Full Text] [PDF]
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 N. Nakao, T. Kurokawa, T. Nonami, G. Tumurkhuu, N. Koide, and T. Yokochi Hydrogen peroxide induces the production of tumor necrosis factor-{alpha} in RAW 264.7 macrophage cells via activation of p38 and stress-activated protein kinase Innate Immunity, June 1, 2008; 14(3): 190 - 196. [Abstract] [PDF]
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N. Sud, S. M. Wells, S. Sharma, D. A. Wiseman, J. Wilham, and S. M. Black Asymmetric dimethylarginine inhibits HSP90 activity in pulmonary arterial endothelial cells: role of mitochondrial dysfunction Am J Physiol Cell Physiol, June 1, 2008; 294(6): C1407 - C1418. [Abstract] [Full Text] [PDF]
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V. G. DeMarco, J. Habibi, A. T. Whaley-Connell, R. I. Schneider, R. L. Heller, J. P. Bosanquet, M. R. Hayden, K. Delcour, S. A. Cooper, B. T. Andresen, et al. Oxidative stress contributes to pulmonary hypertension in the transgenic (mRen2)27 rat Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2659 - H2668. [Abstract] [Full Text] [PDF]
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K. Fujita, N. Maeda, M. Sonoda, K. Ohashi, T. Hibuse, H. Nishizawa, M. Nishida, A. Hiuge, A. Kurata, S. Kihara, et al. Adiponectin Protects Against Angiotensin II-Induced Cardiac Fibrosis Through Activation of PPAR-{alpha} Arterioscler Thromb Vasc Biol, May 1, 2008; 28(5): 863 - 870. [Abstract] [Full Text] [PDF]
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M. Medhora, Y. Chen, S. Gruenloh, D. Harland, S. Bodiga, J. Zielonka, D. Gebremedhin, Y. Gao, J. R. Falck, S. Anjaiah, et al. 20-HETE increases superoxide production and activates NAPDH oxidase in pulmonary artery endothelial cells Am J Physiol Lung Cell Mol Physiol, May 1, 2008; 294(5): L902 - L911. [Abstract] [Full Text] [PDF]
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T. Hayashi, C. Yamashita, C. Matsumoto, C.-J. Kwak, K. Fujii, T. Hirata, M. Miyamura, T. Mori, A. Ukimura, Y. Okada, et al. Role of gp91phox-containing NADPH oxidase in left ventricular remodeling induced by intermittent hypoxic stress Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2197 - H2203. [Abstract] [Full Text] [PDF]
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J. J. P. Deudero, C. Caramelo, M. C. Castellanos, F. Neria, R. Fernandez-Sanchez, O. Calabia, S. Penate, and F. R. Gonzalez-Pacheco Induction of Hypoxia-inducible Factor 1{alpha} Gene Expression by Vascular Endothelial Growth Factor J. Biol. Chem., April 25, 2008; 283(17): 11435 - 11444. [Abstract] [Full Text] [PDF]
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M. Arca, B. Conti, A. Montali, P. Pignatelli, F. Campagna, F. Barilla, G. Tanzilli, R. Verna, A. Vestri, C. Gaudio, et al. C242T Polymorphism of NADPH Oxidase p22phox and Recurrence of Cardiovascular Events in Coronary Artery Disease Arterioscler Thromb Vasc Biol, April 1, 2008; 28(4): 752 - 757. [Abstract] [Full Text] [PDF]
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R. Lopez-Sepulveda, R. Jimenez, M. Romero, M. J. Zarzuelo, M. Sanchez, M. Gomez-Guzman, F. Vargas, F. O'Valle, A. Zarzuelo, F. Perez-Vizcaino, et al. Wine Polyphenols Improve Endothelial Function in Large Vessels of Female Spontaneously Hypertensive Rats Hypertension, April 1, 2008; 51(4): 1088 - 1095. [Abstract] [Full Text] [PDF]
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A. T. Baumer, H. ten Freyhaus, H. Sauer, M. Wartenberg, K. Kappert, P. Schnabel, C. Konkol, J. Hescheler, M. Vantler, and S. Rosenkranz Phosphatidylinositol 3-Kinase-dependent Membrane Recruitment of Rac-1 and p47phox Is Critical for {alpha}-Platelet-derived Growth Factor Receptor-induced Production of Reactive Oxygen Species J. Biol. Chem., March 21, 2008; 283(12): 7864 - 7876. [Abstract] [Full Text] [PDF]
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J. M. Moreno, I. Rodriguez Gomez, R. Wangensteen, M. Alvarez-Guerra, J. d. D. Luna, J. Garcia-Estan, and F. Vargas Tempol improves renal hemodynamics and pressure natriuresis in hyperthyroid rats Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2008; 294(3): R867 - R873. [Abstract] [Full Text] [PDF]
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D. Gozal and L. Kheirandish-Gozal Cardiovascular Morbidity in Obstructive Sleep Apnea: Oxidative Stress, Inflammation, and Much More Am. J. Respir. Crit. Care Med., February 15, 2008; 177(4): 369 - 375. [Abstract] [Full Text] [PDF]
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J. C. Lee, F. Bhora, J. Sun, G. Cheng, E. Arguiri, C. C. Solomides, S. Chatterjee, and M. Christofidou-Solomidou Dietary flaxseed enhances antioxidant defenses and is protective in a mouse model of lung ischemia-reperfusion injury Am J Physiol Lung Cell Mol Physiol, February 1, 2008; 294(2): L255 - L265. [Abstract] [Full Text] [PDF]
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T. Nakamura, E. Yamamoto, K. Kataoka, T. Yamashita, Y. Tokutomi, Y.-F. Dong, S. Matsuba, H. Ogawa, and S. Kim-Mitsuyama Beneficial Effects of Pioglitazone on Hypertensive Cardiovascular Injury Are Enhanced by Combination With Candesartan Hypertension, February 1, 2008; 51(2): 296 - 301. [Abstract] [Full Text] [PDF]
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Y. H. Looi, D. J. Grieve, A. Siva, S. J. Walker, N. Anilkumar, A. C. Cave, M. Marber, M. J. Monaghan, and A. M. Shah Involvement of Nox2 NADPH Oxidase in Adverse Cardiac Remodeling After Myocardial Infarction Hypertension, February 1, 2008; 51(2): 319 - 325. [Abstract] [Full Text] [PDF]
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A. Yogi, C. Mercure, J. Touyz, G. E. Callera, A. C.I. Montezano, A. B. Aranha, R. C. Tostes, T. Reudelhuber, and R. M. Touyz Renal Redox-Sensitive Signaling, but Not Blood Pressure, Is Attenuated by Nox1 Knockout in Angiotensin II-Dependent Chronic Hypertension Hypertension, February 1, 2008; 51(2): 500 - 506. [Abstract] [Full Text] [PDF]
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S. Yagi, K.-i. Aihara, Y. Ikeda, Y. Sumitomo, S. Yoshida, T. Ise, T. Iwase, K. Ishikawa, H. Azuma, M. Akaike, et al. Pitavastatin, an HMG-CoA Reductase Inhibitor, Exerts eNOS-Independent Protective Actions Against Angiotensin II Induced Cardiovascular Remodeling and Renal Insufficiency Circ. Res., January 4, 2008; 102(1): 68 - 76. [Abstract] [Full Text] [PDF]
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Y. M. Kim, H. Kattach, C. Ratnatunga, R. Pillai, K. M. Channon, and B. Casadei Association of atrial nicotinamide adenine dinucleotide phosphate oxidase activity with the development of atrial fibrillation after cardiac surgery. J. Am. Coll. Cardiol., January 1, 2008; 51(1): 68 - 74. [Abstract] [Full Text] [PDF]
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J. C. Velasquez-Castano and W. R. Taylor Angiotensin II and New Vessel Formation: Aiming for the Right Oxidative Window Arterioscler Thromb Vasc Biol, January 1, 2008; 28(1): 4 - 5. [Full Text] [PDF]
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F. Jiang, N. Guo, and G. J. Dusting Modulation of Nicotinamide Adenine Dinucleotide Phosphate Oxidase Expression and Function by 3',4'-Dihydroxyflavonol in Phagocytic and Vascular Cells J. Pharmacol. Exp. Ther., January 1, 2008; 324(1): 261 - 269. [Abstract] [Full Text] [PDF]
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R. Reed, C. Kolz, B. Potter, and P. Rocic The Mechanistic Basis for the Disparate Effects of Angiotensin II on Coronary Collateral Growth Arterioscler Thromb Vasc Biol, January 1, 2008; 28(1): 61 - 67. [Abstract] [Full Text] [PDF]
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A. R. Hemnes, A. Zaiman, and H. C. Champion PDE5A inhibition attenuates bleomycin-induced pulmonary fibrosis and pulmonary hypertension through inhibition of ROS generation and RhoA/Rho kinase activation Am J Physiol Lung Cell Mol Physiol, January 1, 2008; 294(1): L24 - L33. [Abstract] [Full Text] [PDF]
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S. Li, X. Li, H. Zheng, B. Xie, K. R. Bidasee, and G. J. Rozanski Pro-oxidant effect of transforming growth factor-{beta}1 mediates contractile dysfunction in rat ventricular myocytes Cardiovasc Res, January 1, 2008; 77(1): 107 - 117. [Abstract] [Full Text] [PDF]
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A. Vinh, R. E. Widdop, G. R. Drummond, and T. A. Gaspari Chronic angiotensin IV treatment reverses endothelial dysfunction in ApoE-deficient mice Cardiovasc Res, January 1, 2008; 77(1): 178 - 187. [Abstract] [Full Text] [PDF]
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A. E. Vendrov, Z. S. Hakim, N. R. Madamanchi, M. Rojas, C. Madamanchi, and M. S. Runge Atherosclerosis Is Attenuated by Limiting Superoxide Generation in Both Macrophages and Vessel Wall Cells Arterioscler Thromb Vasc Biol, December 1, 2007; 27(12): 2714 - 2721. [Abstract] [Full Text] [PDF]
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D. D. Lund, R. M. Brooks, F. M. Faraci, and D. D. Heistad Role of angiotensin II in endothelial dysfunction induced by lipopolysaccharide in mice Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3726 - H3731. [Abstract] [Full Text] [PDF]
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R. S. Arnold, J. He, A. Remo, D. Ritsick, Q. Yin-Goen, J. D. Lambeth, M. W. Datta, A. N. Young, and J. A. Petros Nox1 Expression Determines Cellular Reactive Oxygen and Modulates c-fos-Induced Growth Factor, Interleukin-8, and Cav-1 Am. J. Pathol., December 1, 2007; 171(6): 2021 - 2032. [Abstract] [Full Text] [PDF]
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T. Korff, K. Aufgebauer, and M. Hecker Cyclic Stretch Controls the Expression of CD40 in Endothelial Cells by Changing Their Transforming Growth Factor-{beta}1 Response Circulation, November 13, 2007; 116(20): 2288 - 2297. [Abstract] [Full Text] [PDF]
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W. Ni, Y. Zhan, H. He, E. Maynard, J. A. Balschi, and P. Oettgen Ets-1 Is a Critical Transcriptional Regulator of Reactive Oxygen Species and p47phox Gene Expression in Response to Angiotensin II Circ. Res., November 9, 2007; 101(10): 985 - 994. [Abstract] [Full Text] [PDF]
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K. K. Ogden, J. R. Falck, and S. W. Watts The Cytochrome P450 Inhibitor Ketoconazole Potentiates 5-Hydroxytryptamine-Induced Contraction in Rat Aorta J. Pharmacol. Exp. Ther., November 1, 2007; 323(2): 606 - 613. [Abstract] [Full Text] [PDF]
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A. Dandapat, C. Hu, L. Sun, and J. L. Mehta Small Concentrations of oxLDL Induce Capillary Tube Formation From Endothelial Cells via LOX-1 Dependent Redox-Sensitive Pathway Arterioscler Thromb Vasc Biol, November 1, 2007; 27(11): 2435 - 2442. [Abstract] [Full Text] [PDF]
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S. R. Datla, H. Peshavariya, G. J. Dusting, K. Mahadev, B. J. Goldstein, and F. Jiang Important Role of Nox4 Type NADPH Oxidase in Angiogenic Responses in Human Microvascular Endothelial Cells In Vitro Arterioscler Thromb Vasc Biol, November 1, 2007; 27(11): 2319 - 2324. [Abstract] [Full Text] [PDF]
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R. K. Upmacis, M. J. Crabtree, R. S. Deeb, H. Shen, P. B. Lane, L. E. S. Benguigui, N. Maeda, D. P. Hajjar, and S. S. Gross Profound biopterin oxidation and protein tyrosine nitration in tissues of ApoE-null mice on an atherogenic diet: contribution of inducible nitric oxide synthase Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H2878 - H2887. [Abstract] [Full Text] [PDF]
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T. Hashimoto, M. Kihara, N. Imai, S.-i. Yoshida, H. Shimoyamada, H. Yasuzaki, J. Ishida, Y. Toya, Y. Kiuchi, N. Hirawa, et al. Requirement of Apelin-Apelin Receptor System for Oxidative Stress-Linked Atherosclerosis Am. J. Pathol., November 1, 2007; 171(5): 1705 - 1712. [Abstract] [Full Text] [PDF]
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T. Nakamura, E. Yamamoto, K. Kataoka, T. Yamashita, Y. Tokutomi, Y.-F. Dong, S. Matsuba, H. Ogawa, and S. Kim-Mitsuyama Pioglitazone Exerts Protective Effects Against Stroke in Stroke-Prone Spontaneously Hypertensive Rats, Independently of Blood Pressure Stroke, November 1, 2007; 38(11): 3016 - 3022. [Abstract] [Full Text] [PDF]
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G.-X. Zhang, X.-M. Lu, S. Kimura, and A. Nishiyama Role of mitochondria in angiotensin II-induced reactive oxygen species and mitogen-activated protein kinase activation Cardiovasc Res, November 1, 2007; 76(2): 204 - 212. [Abstract] [Full Text] [PDF]
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Y. C. Chan and P. S. Leung Angiotensin II Type 1 Receptor-Dependent Nuclear Factor-{kappa}B Activation-Mediated Proinflammatory Actions in a Rat Model of Obstructive Acute Pancreatitis J. Pharmacol. Exp. Ther., October 1, 2007; 323(1): 10 - 18. [Abstract] [Full Text] [PDF]
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Y. Li and H. E. Schellhorn New Developments and Novel Therapeutic Perspectives for Vitamin C J. Nutr., October 1, 2007; 137(10): 2171 - 2184. [Abstract] [Full Text] [PDF]
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S. A. Cooper, A. Whaley-Connell, J. Habibi, Y. Wei, G. Lastra, C. Manrique, S. Stas, and J. R. Sowers Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2009 - H2023. [Abstract] [Full Text] [PDF]
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