Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation Research
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Circulation Research. 2004;95:671-676
doi: 10.1161/01.RES.0000143421.27684.12
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Abedin, M.
Right arrow Articles by Demer, L. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Abedin, M.
Right arrow Articles by Demer, L. L.
Related Collections
Right arrow Mechanism of atherosclerosis/growth factors
Right arrow Other Vascular biology
(Circulation Research. 2004;95:671.)
© 2004 American Heart Association, Inc.

Reviews

Mesenchymal Stem Cells and the Artery Wall

Moeen Abedin, Yin Tintut, Linda L. Demer

From the Departments of Medicine and Physiology, The David Geffen School of Medicine at University of California at Los Angeles.

Correspondence to Linda L. Demer, MD, PhD, 47-123 CHS, The David Geffen School of Medicine at UCLA, 10833 LeConte Ave, Los Angeles, CA 90095-1679. E-mail LDemer{at}mednet.ucla.edu

This Review is part of a thematic series on Mechanisms of Vascular Calcification, which includes the following articles:

Pathophysiology of Vascular Calcification in Chronic Kidney Disease

Mesenchymal Stem Cells and the Artery Wall

Angiogenesis and Pericytes in Initiation of Ectopic Calcification

Osteopontin Promoter Regulation and Phosphate Transport Molecules in Vascular Calcification

Regulation of Vascular Calcification by Osteoclast Regulatory Factors RANKL and Osteoprotegerin

Role of Bone Morphogenetic Proteins in Vascular Calcification
Linda Demer Guest Editor


*    Abstract
up arrowTop
 *Abstract
down arrowIntroduction
 down arrowMesenchymal Stem Cells
 down arrowEngraftment
 down arrowEndothelial Progenitor Cells
 down arrowSummary
 down arrowReferences
 
The presence of ectopic tissue in the diseased artery wall is evidence for the presence of multipotential stem cells in the vasculature. Mesenchymal stem cells were first identified in the marrow stroma, and they differentiate along multiple lineages giving rise to cartilage, bone, fat, muscle, and vascular tissue in vitro and in vivo. Transplantation studies show that marrow-derived mesenchymal stem cells appear to enter the circulation and engraft other tissues, including the artery wall, at sites of injury. Recent evidence indicates that mesenchymal stem cells are also present in normal artery wall and microvessels and that they also may enter the circulation, contributing to the population of circulating progenitor cells and engrafting other tissues. Thus, the artery wall is not only a destination but also a source of progenitor cells that have regenerative potential. Although potential artifacts, such as fusion, need to be taken into consideration, these new developments in vascular biology open important therapeutic avenues. A greater understanding of how mesenchymal stem cells from the bone marrow or artery wall bring about vascular regeneration and repair may lead to novel cell-based treatments for cardiovascular disease.


Key Words: vascular • mesenchymal stem cell • calcification • bone • atherosclerosis


*    Introduction
up arrowTop
 up arrowAbstract
 *Introduction
down arrowMesenchymal Stem Cells
 down arrowEngraftment
 down arrowEndothelial Progenitor Cells
 down arrowSummary
 down arrowReferences
 
Multilineage tissue is well known to develop in the human artery wall, especially in association with atherosclerotic lesions. First described by pathologists centuries ago, the phenomenon has been termed metaplasia, and it appears in the form of ectopic cartilage, bone, fat, and marrow.1–6 Its significance as evidence for mesenchymal stem cells (MSCs) in the artery wall has not been appreciated until recently.

Mature bone tissue is found in 5% to 20% of atherosclerotic arteries,4,7 although earlier stages may occur more often.8 Hematopoietic marrow has been found in artery walls of 9 of 200 cases.4 Cartilage tissue is also found within human atherosclerotic plaque,9 but its frequency has not been systematically assessed. Ectopic tissue occurs in veins as well as arteries10 and in animal models of atherosclerosis.11 In mice, vascular ectopic tissue is most often in the form of cartilage.9,12–15

Osteogenic and chondrogenic differentiation in the artery wall are recognized clinically as vascular calcification and are detectable by x-ray, computed tomographic scanning, or ultrasound. Such mineralization is associated with increased cardiovascular morbidity and mortality.16–19 On the basis of physiological experiments, vascular calcification is known to increase aortic stiffness, resulting in systolic hypertension, coronary insufficiency, left ventricular hypertrophy, ischemia, and congestive heart failure.20–22 Although plaque surrounded by a calcium deposit is under reduced mechanical stress because of load sharing, failure stress is increased at the interface of the calcium deposit with soft tissue, increasing the likelihood of tissue rupture at those edges. Approximately 85% of plaques causing coronary thrombosis are calcified.23


*    Mesenchymal Stem Cells
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 *Mesenchymal Stem Cells
down arrowEngraftment
 down arrowEndothelial Progenitor Cells
 down arrowSummary
 down arrowReferences
 
In pioneering work, Prockop et al showed that transplanted marrow cells engraft connective tissues such as spleen and liver.24,25 Liechty et al showed that human marrow cells engraft multiple tissues when injected in utero in sheep.26 The concept of a continuous replacement of connective tissue with marrow cells parallels the known continuous replacement of blood by bone marrow hematopoietic cells.

For hematopoietic stem cells, lineage acquisition is regulated by well-defined colony-stimulating factors. Little is known about the corresponding regulatory mechanisms for MSCs. Hematopoietic stem cells were first found in the marrow. They are now harvested from peripheral blood for clinical regeneration of marrow. MSCs were also first identified in the marrow, and they are now harvested from a variety of tissue sources.27–32 It has been suggested that MSCs serve as universal repair cells in adult tissues as they undergo regeneration or remodeling.33,34

MSCs in Bone Marrow
Marrow stromal cells, a subpopulation of nonhematopoietic cells in the bone marrow, are the prototypical MSCs.35 They represent a small percentage of marrow cells, and they can be partially distinguished from hematopoeitic cells by their ability to adhere to tissue culture dishes. In culture, they may be guided to differentiate into bone, fat, cartilage, or muscle cells using specific media.34,36–38 When cultured in ordinary media containing 10% to 20% fetal serum, they form multiple clusters of different lineages within a single dish.39 They are guided into specific, single-lineage differentiation by culture in serum-free "induction media" containing growth factors and other treatments such as insulin, dexamethasone, and indomethacin.36 Recent evidence indicates that even marrow MSCs that have already fully differentiated into 1 lineage are capable of transdifferentiation into another lineage in response to induction media.40 Marrow MSCs also maintain multipotential capacity in vivo, tending to differentiate into the cell type of the tissue they engraft.26 This tendency to adopt local identity may be directed by local cytokines and matrix factors from host cells. Thus, adequate contact with host cells may be required to ensure that engrafted cells assume host tissue identity rather than differentiating along other mesenchymal lineages.

Importantly, the evidence that marrow MSCs transdifferentiate to adopt local tissue identity may be confounded by the phenomenon of cell fusion. In this process, a labeled donor cell fuses with a differentiated host cell, resulting in a cell positive for label and differentiation marker, falsely indicating transdifferentiation. To date, artifact attributable to cell fusion has been an issue in studies of nonvascular tissues, but in principal, it may occur in any cell type.41,42

Marrow-derived MSCs also have vascular differentiation potential. In culture, they differentiate into smooth muscle cells (SMCs).27,43 In vivo, bone marrow–derived cells that were seeded on a synthetic vascular graft produced smooth muscle and endothelial layers.44 Although it is attractive to consider that growth of MSCs in injured vascular tissue may simply regenerate normal vascular tissue, it is also possible for these cells to produce ectopic tissues, such as those seen in advanced atherosclerotic calcification. In addition, although marrow cell–induced changes may result directly from assimilation of marrow cells, the benefit may also be an indirect, paracrine effect of cytokines released by the marrow-derived cells. The factors governing these possibilities are not clear, but it appears that metabolic diseases, such as atherosclerosis or diabetes, favor the formation of ectopic tissue.

MSCs in Arteries
The tunica media has been widely perceived as a homogeneous, terminally differentiated layer of SMCs. However, many investigators have shown that cultured SMCs are heterogeneous45,46 and that they undergo dedifferentiation in culture.47–49 Interestingly, vascular SMCs were described as "multifunctional mesenchymal cells" 36 years ago,50 foreshadowing the finding of multipotential mesenchymal cells as subpopulations of SMCs within the artery wall.

Osteoblastic Differentiation of Vascular Cells
The first evidence that SMCs undergo osteoblastic differentiation was the production of calcified nodules by cultured microvascular pericytes.51 Similar calcified nodules were found in a subpopulation of aortic SMCs with pericyte-like features (calcifying vascular cells [CVCs]). These cells and SMCs express osteoblastic-specific genes52–58 in a time course characteristic of bone cell differentiation.59 Osteoblastic differentiation also has been shown in cultures of cardiac valvular cells,60,61 which may account for the formation of bone in stenotic aortic valves.

Multilineage Differentiation of Vascular Cells
Pericytes and SMCs were known to have chondrogenic features,62,63 and their multilineage potential has now been shown in vitro54,64 and in vivo.65 The lineage repertoires for the 2 cell types appear to differ slightly. Both express markers specific for chondroblasts, osteoblasts, and smooth muscle. In addition, pericytes also undergo adipogenic differentiation, whereas CVCs can undergo marrow stromal differentiation. This difference in plasticity may be attributable to technical differences or have biological significance. One possibility is that the pericytes are harvested from retinal vessels, which derive from neural crest, whereas CVCs are harvested from descending aorta, which is believed to derive from non–neural crest mesenchyme. Pericytes and CVCs are distinguished from other vascular SMCs by their expression of a surface ganglioside recognized by a monoclonal antibody (3G5).52,64,66 Pericyte-like cells from the human umbilical vein also form fibroblastoid cell colonies and express osteogenic, chondrogenic, and adipogenic markers.67 It has been suggested that although pericytes have been defined by their location in the microvessels, pericyte-like cells are also present in large arteries, and they form an anatomically continuous network in the subendothelial space.68 Importantly, the other tissues that have been shown to contain MSCs also contain substantial vascular or microvascular tissue. This suggests the concept that pericyte-like vascular cells account for the multilineage potential in fat, skeletal muscle, and other tissues.

Regulation of Vascular Stem Cell Lineage
Factors regulating differentiation of these cells remain under investigation. Bone morphogenetic protein-2 is a candidate on the basis of its ability to regulate mesenchymal lineage in neural crest cells. This potent embryonic differentiation factor from the transforming growth factor-ß superfamily is best known for promoting osteogenic differentiation, but it modulates the entire spectrum of mesenchymal lineages. Multipotent, mouse embryonic mesenchymal (C3H10T1/2) cells undergo chondrogenic differentiation at high levels of BMP-2, osteogenic differentiation at lower levels, smooth muscle or adipogenic differentiation at even lower levels, and little or no differentiation in the absence of BMP-2.69,70 Adult vascular MSCs organize themselves into intricate patterns in culture. These patterns are generated by a reaction-diffusion process, which is driven by the interaction of BMP-2 activity with its more rapidly diffusing inhibitor matrix Gla protein.71 The Wnt family of transcription factors, which interacts with BMP-2 in determining mesenchymal lineage in embryonic neural crest cells,72 may also regulate differentiation of adult vascular stem cells. These findings suggest that BMP-2 and associated factors regulate the formation of complex mesenchymal structures in vivo, and their control will be important in future tissue engineering.

It is not clear why MSCs undergo multilineage differentiation in vitro, whereas they normally remain undifferentiated or produce daughter cells that differentiate only along the same lineage as the surrounding tissue in vivo. In the native environment, neighboring cells or matrix may send instructive signals that are absent in culture. Extracellular matrix regulates differentiation,73 and it may maintain progenitor cells in a quiescent state until the tissue architecture is disrupted. Consistent with an environmental effect, saphenous veins rarely develop calcification, but 11% of vein grafts mineralize after they are exposed to arterial circulation as coronary bypass grafts.74 Even more rapid mineralization, in the form of cartilage and bone, occurs in mice undergoing carotid interposition surgery.75


*    Engraftment
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMesenchymal Stem Cells
 *Engraftment
down arrowEndothelial Progenitor Cells
 down arrowSummary
 down arrowReferences
 
Engraftment by Marrow MSCs
In human gender-mismatched bone marrow transplant recipients, donor marrow cells engraft all layers of atherosclerotic plaques76 but not disease-free segments, suggesting that engraftment may require inflammation or injury. Similarly, in mice with atherosclerosis, labeled donor marrow cells engraft plaque. Interestingly, recipients have less atherosclerosis when donor marrow-derived progenitor cells are from young versus older mice.77

In transplanted hearts, a neointima forms throughout the coronaries of the transplanted heart, leading to diffuse transplant coronary arteriopathy and often ischemia. The neointima was originally believed to derive locally from the donor tunica media. However, studies in mouse cardiovascular transplant models have shown that much of the neointima derived from the host.78,79 When labeled veins are transplanted into the carotids of unlabeled recipient mice, the label disappears over time, suggesting engraftment by circulating host cells; conversely, unlabeled donor veins transplanted into labeled recipients gain label, again suggesting engraftment by host cells.80 Although these results could be explained by local migration of vascular cells, the changes in labeling occurred uniformly throughout the graft rather than predominantly at the edges, supporting a circulatory origin for the engrafting cells. Because circulating cells include hematopoeitic as well as mesenchymal cells, some instances of host cell "engraftment" may be attributable to ordinary diapedesis by host leukocytes, especially in areas of inflammation or injury.81 To exclude this possibility, label and phenotypic markers should be assessed in studies of mesenchymal cell engraftment.

In some experimental conditions, even injured vascular tissue is not engrafted by marrow cells.82 Location and type of injury may determine whether marrow cells engraft.83 External injury by cuff or ligation in mice stimulates little neointimal and rare SMC layer engraftment, whereas internal injury by femoral wire denudation induces substantial neointimal (40%) and SMC (25%) engraftment.84 Thus, technical differences may affect results of engraftment studies and need to be taken into consideration in future clinical applications.

Engraftment by Vascular Cells
Some of the first evidence for engraftment by vascular cells came from Campbell et al, who implanted a prosthetic scaffold in the peritoneum and found endothelial and SMC attachment and growth.85 Similar engraftment was found in vascular prosthetic scaffolds.84,86 Recent in vivo studies indicate that vascular cells can emigrate from the artery wall and migrate to remote tissues, presumably through the circulation. Montfort et al transplanted aortic segments from labeled donors into the kidney capsule of recipients and found engraftment of donor vascular cells in the recipient spleen with evidence of differentiation into marrow stromal cells.87 This important observation suggests that vascular cells may migrate from their tissue location and enter the circulation, opening possibilities for new pathophysiological mechanisms.

Although the marrow and the circulation are considered distinct compartments or sources of cells, they may overlap substantially, given that marrow-derived progenitor cells may travel in the circulation before arriving at their engraftment destination. Thus, peripheral blood mononuclear cells (PBMCs) and other circulating progenitor cells may originate from other mesenchymal tissues besides the marrow.


*    Endothelial Progenitor Cells
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMesenchymal Stem Cells
 up arrowEngraftment
 *Endothelial Progenitor Cells
down arrowSummary
 down arrowReferences
 
Endothelial Progenitor Cells in Circulation
PBMCs differentiate not only into lymphocytes and monocytes but also into endothelial and SMCs. When cultured on type I collagen in endothelial growth medium (EGM) with platelet-derived growth factor-BB, PBMCs express SMC markers. Those cultured in EGM alone also develop an endothelial cell (EC) phenotype.88 Endothelial progenitor cells (EPCs) can be isolated directly from PBMC by flow cytometric sorting using surface markers such as CD34, a marker associated previously with hematopoietic stem cells. This intriguing sharing of markers may reflect the embryonic origin of ECs from hemangioblasts, cells with hematopoietic and endothelial potential. When circulating EPCs are injected into rabbits at the time of arterial injury, they engraft the injured vascular sites.89 EPCs promote neoangiogenesis in myocardial ischemia90 and re-endothelialize large vessel injuries.91 Skeletal muscle tissue contains EPCs that differentiate into ECs at the site of muscle injury.92 Thus, EPCs may account for spontaneous regeneration of endothelium in injured or transplanted tissue.

Factors Affecting EPC Numbers
The numbers of EPCs present in the circulation are affected by lipids, estrogen status, erythropoietin, exercise, coronary risk status, and progressive cancer. Hyperlipidemia reduces the EPC numbers and engraftment potential in mice.80 Mice treated with a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor had increased numbers of circulating cells positive for markers Sca-1 and vascular endothelial growth factor-2R.93 Women with higher plasma estrogen levels have more circulating EPCs, whereas ovariectomized mice have fewer EPCs and more neointima after carotid balloon injury.94 In patients with end-stage renal disease, treatment with erythropoietin was associated with increased numbers of CD34+ blood cells and increased endothelial differentiation of those cells in vitro.95 EPC numbers, measured as colony-forming units, also correlate inversely with Framingham risk score in humans,96 and they are increased by exercise in mice and humans.97 Importantly, EPC numbers are also increased in the circulation in cancer patients,98 raising the possibility that availability of EPCs may be permissive for tumor neoangiogenesis and growth.

Teleology
What would be the teleological basis for inflammation-induced ectopic differentiation of MSCs? It may be adaptive, as part of a defense against chronic infection. It is not unusual to find, deep in the middle of a soft tissue organ, a layer of bone surrounding an abscess, tuberculoma, or parasite. When leukocytes attack a pathogen, they release free radicals that oxidatively modify lipids in the pathogen membrane and surrounding tissue to a more inflammatory form.99,100 When the pathogen is not eliminated, these persistent inflammatory lipids may serve as a signal to local MSCs that the infection remains and triggers a more definitive immune response, such as encasement by ectopic bone to isolate the infectious process. With modern high-fat diets, hyperlipidemia results in deposition of lipoproteins in perivascular spaces of soft tissues, and these undergo partial nonenzymatic oxidation. Vascular MSCs may misinterpret these mildly oxidized lipids as evidence of persistent infectious organisms and respond by attempting to sequester them in a wall of bone or cartilage.


*    Summary
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMesenchymal Stem Cells
 up arrowEngraftment
 up arrowEndothelial Progenitor Cells
 *Summary
down arrowReferences
 
New evidence suggests that the artery wall is a recipient and source of MSCs. The long-recognized formation of ectopic mesenchymal tissue in the artery wall was a clue that MSCs are present in the adult artery wall. These stem cells, which were first identified in the marrow stroma, can differentiate along multiple lineages and give rise to cartilage, bone, fat, muscle, and vascular tissue in vitro and in vivo. Similar cells with multilineage and self-renewal capacity have also been harvested and cultured from muscle, blood, fat, and now adult vascular tissue. PBMCs also may serve as progenitors for endothelium and possibly smooth muscle. Marrow cells appear to enter the circulation and engraft vascular and other connective tissues, especially at sites of injury and in tissue transplant grafts. Conversely, provocative evidence suggests that cells from vascular tissue may enter the circulation and engraft remote organs. Yet, the possibility remains that MSCs from the bone marrow or the artery wall may permit human tissue regeneration and repair, an exciting future prospect for cardiovascular disease.


*    Acknowledgments
 
We are grateful for the support of the National Institutes of Health/National Heart, Lung, and Blood Institute/National Institute of Arthritis and Musculoskeletal and Skin Diseases (HL/AR 69261) and the Laubisch Fund.


*    Footnotes
 
Original received June 14, 2004; revision received August 17, 2004; accepted August 17, 2004.


*    References
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMesenchymal Stem Cells
 up arrowEngraftment
 up arrowEndothelial Progenitor Cells
 up arrowSummary
 *References
 

  1. Hull G. Caleb Hillier Parry 1755–1822: a notable provincial physician. J R Soc Med. 1998; 91: 335–338.[Medline] [Order article via Infotrieve]
  2. Virchow R. Cellular Pathology. New York, NY: Dover; 1863.
  3. Jeziorska M, McCollum C, Wooley DE. Observations on bone formation and remodeling in advanced atherosclerotic lesions of human carotid arteries. Virchows Arch. 1998; 433: 559–565.[CrossRef][Medline] [Order article via Infotrieve]
  4. Seemayer TA, Thelmo WL, Morin J. Cartilaginous transformation of the aortic valve. Am J Clin Pathol. 1973; 60: 616–620.[Medline] [Order article via Infotrieve]
  5. Bunting CH. The formation of true bone with cellular (red) marrow in a sclerotic aorta. Journal of Experimental Medicine. 1906; 8: 365–376.[CrossRef]
  6. Buerger L, Oppenheimer A. Bone formation in sclerotic arteries. J Exp Med. 1908; 10: 354–367.[CrossRef]
  7. Hunt JL, Fairman R, Mitchell ME, Carpenter JP, Golden M, Khalapyan T, Wolfe M, Neschis D, Milner R, Scoll B, Cusack A, Mohler ER III. Bone formation in carotid plaques: a clinicopathological study. Stroke. 2002; 33: 1214–1219.[Abstract/Free Full Text]
  8. Christian RC, Fitzpatrick LA. Vascular calcification. Curr Opin Nephrol Hypertens. 1999; 8: 443–448.[CrossRef][Medline] [Order article via Infotrieve]
  9. Qiao JH, Mertens RB, Fishbein MC, Geller SA. Cartilaginous metaplasia in calcified diabetic peripheral vascular disease: morphologic evidence of enchondral ossification. Hum Pathol. 2003; 34: 402–407.[CrossRef][Medline] [Order article via Infotrieve]
  10. Stehbens WE. Chronic vascular changes in the walls of experimental berry aneurysms of the aortic bifurcation in rabbits. Stroke. 1981; 12: 643–647.[Abstract/Free Full Text]
  11. Haust D, More RH. Spontaneous Lesions of the Aorta in the Rabbit. New York, NY: Harper and Row; 1965.
  12. Hadjiisky P, Donev S, Renais J, Scebat L. Cartilage and bone formation in arterial wall. 1. Morphological and histochemical aspects. Basic Res Cardiol. 1979; 74: 649–662.[CrossRef][Medline] [Order article via Infotrieve]
  13. Hadjiisky P, Donev S, Renais J, Scebat L. Cartilage and bone formation in arterial wall. 2. Ultrastructural patterns. Basic Res Cardiol. 1980; 75: 365–367.[CrossRef][Medline] [Order article via Infotrieve]
  14. Rosenfeld ME, Polinsky P, Virmani R, Kauser K, Rubanyi G, Schwartz SM. Advanced atherosclerotic lesions in the innominate artery of the ApoE knockout mouse. Arterioscler Thromb Vasc Biol. 2000; 20: 2587–2592.[Abstract/Free Full Text]
  15. Tse J, Martin-McNaulty B, Halks-Miller M, Kauser K, DelVecchio V, Vergona R, Sullivan ME, Rubanyi GM. Accelerated atherosclerosis and premature calcified cartilaginous metaplasia in the aorta of diabetic male Apo E knockout mice can be prevented by chronic treatment with 17 beta-estradiol. Atherosclerosis. 1999; 144: 303–313.[CrossRef][Medline] [Order article via Infotrieve]
  16. Wayhs R, Zelinger A, Raggi P. High coronary artery calcium scores pose an extremely elevated risk for hard events. J Am Coll Cardiol. 2002; 39: 225–230.[Abstract/Free Full Text]
  17. Arad Y, Spadaro LA, Goodman K, Newstein D, Guerci AD. Prediction of coronary events with electron beam computed tomography. J Am Coll Cardiol. 2000; 36: 1253–1260.[Abstract/Free Full Text]
  18. Keelan PC, Bielak LF, Ashai K, Jamjoum LS, Denktas AE, Rumberger JA, Sheedy IP, Peyser PA, Schwartz RS. Long-term prognostic value of coronary calcification detected by electron-beam computed tomography in patients undergoing coronary angiography. Circulation. 2001; 104: 412–417.[Abstract/Free Full Text]
  19. Wong ND, Detrano RC, Diamond G, Rezayat C, Mahmoudi R, Chong EC, Tang W, Puentes G, Kang X, Abrahamson D. Does coronary artery screening by electron beam computed tomography motivate potentially beneficial lifestyle behaviors? Am J Cardiol. 1996; 78: 1220–1223.[CrossRef][Medline] [Order article via Infotrieve]
  20. Kelly RP, Tunin R, Kass DA. Effect of reduced aortic compliance on cardiac efficiency and contractile function of in situ canine left ventricle. Circ Res. 1992; 71: 490–502.[Abstract/Free Full Text]
  21. Ohtsuka S, Kakihana M, Watanabe H, Sugishita Y. Chronically decreased aortic distensibility causes deterioration of coronary perfusion during increased left ventricular contraction. J Am Coll Cardiol. 1994; 24: 1406–1414.[Abstract]
  22. Watanabe H, Ohtsuka S, Kakihana M, Sugishita Y. Decreased aortic compliance aggravates subendocardial ischaemia in dogs with stenosed coronary artery. Cardiovasc Res. 1992; 26: 1212–1218.[Abstract/Free Full Text]
  23. Richardson PD, Davies MJ, Born GV. Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet. 1989; 2: 941–944.[CrossRef][Medline] [Order article via Infotrieve]
  24. Prockop DJ. Marrow stromal cells as stem cells for nonhematopoietic tissues. Science. 1997; 276: 71–74.[Abstract/Free Full Text]
  25. Prockop DJ. Marrow stromal cells as stem cells for continual renewal of nonhematopoietic tissues and as potential vectors for gene therapy. J Cell Biochem Suppl. 1998; 30–31: 284–285.
  26. Liechty KW, MacKenzie TC, Shaaban AF, Radu A, Moseley AM, Deans R, Marshak DR, Flake AW. Human mesenchymal stem cells engraft and demonstrate site-specific differentiation after in utero transplantation in sheep. Nat Med. 2000; 6: 1282–1286.[CrossRef][Medline] [Order article via Infotrieve]
  27. Zuk PA, Zhu M, Mizuno H, Huang J, Futrell JW, Katz AJ, Benhaim P, Lorenz HP, Hedrick MH. Multilineage cells from human adipose tissue: implications for cell-based therapies. Tissue Eng. 2001; 7: 211–228.[CrossRef][Medline] [Order article via Infotrieve]
  28. Mizuno H, Zuk PA, Zhu M, Lorenz HP, Benhaim P, Hedrick MH. Myogenic differentiation by human processed lipoaspirate cells. Plast Reconstr Surg. 2002; 109: 199–209.[CrossRef][Medline] [Order article via Infotrieve]
  29. Arai Y, Hirose N, Yamamura K, Kimura M, Murayama A, Fujii I, Tsushima M. Long-term effect of lipid-lowering therapy on atherosclerosis of abdominal aorta in patients with hypercholesterolemia: noninvasive evaluation by a new image analysis program. Angiology. 2002; 53: 57–68.[Medline] [Order article via Infotrieve]
  30. Wakitani S, Yamamoto T. Response of the donor and recipient cells in mesenchymal cell transplantation to cartilage defect. Microsc Res Tech. 2002; 58: 14–18.[CrossRef][Medline] [Order article via Infotrieve]
  31. Campagnoli C, Roberts IA, Kumar S, Bennett PR, Bellantuono I, Fisk NM. Identification of mesenchymal stem/progenitor cells in human first-trimester fetal blood, liver, and bone marrow. Blood. 2001; 98: 2396–2402.[Abstract/Free Full Text]
  32. Erices A, Conget P, Minguell JJ. Mesenchymal progenitor cells in human umbilical cord blood. Br J Haematol. 2000; 109: 235–242.[CrossRef][Medline] [Order article via Infotrieve]
  33. Ferrari G, Cusella-De Angelis G, Coletta M, Paolucci E, Stornaiuolo A, Cossu G, Mavilio F. Muscle regeneration by bone marrow-derived myogenic progenitors. Science. 1998; 279: 1528–1530.[Abstract/Free Full Text]
  34. Hirschi KK, Goodell MA. Hematopoietic, vascular and cardiac fates of bone marrow-derived stem cells. Gene Ther. 2002; 9: 648–652.[CrossRef][Medline] [Order article via Infotrieve]
  35. Caplan AI. Mesenchymal stem cells. J Orthop Res. 1991; 9: 641–650.[CrossRef][Medline] [Order article via Infotrieve]
  36. Pittenger MF, Mackay AM, Beck SC, Jaiswal RK, Douglas R, Mosca JD, Moorman MA, Simonetti DW, Craig S, Marshak DR. Multilineage potential of adult human mesenchymal stem cells. Science. 1999; 284: 143–147.[Abstract/Free Full Text]
  37. Schwartz RE, Reyes M, Koodie L, Jiang Y, Blackstad M, Lund T, Lenvik T, Johnson S, Hu WS, Verfaillie CM. Multipotent adult progenitor cells from bone marrow differentiate into functional hepatocyte-like cells. J Clin Invest. 2002; 109: 1291–1302.[CrossRef][Medline] [Order article via Infotrieve]
  38. Hirschi K, Goodell M. Common origins of blood and blood vessels in adults? Differentiation. 2001; 68: 186–192.[CrossRef][Medline] [Order article via Infotrieve]
  39. Majumdar MK, Banks V, Peluso DP, Morris EA. Isolation, characterization, and chondrogenic potential of human bone marrow-derived multipotential stromal cells. J Cell Physiol. 2000; 185: 98–106.[CrossRef][Medline] [Order article via Infotrieve]
  40. Song L, Tuan RS. Transdifferentiation potential of human mesenchymal stem cells derived from bone marrow. FASEB J. 2004; 18: 980–982.[Abstract/Free Full Text]
  41. Ying QL, Nichols J, Evans EP, Smith AG. Changing potency by spontaneous fusion. Nature. 2002; 416: 545–548.[CrossRef][Medline] [Order article via Infotrieve]
  42. Terada N, Hamazaki T, Oka M, Hoki M, Mastalerz DM, Nakano Y, Meyer EM, Morel L, Petersen BE, Scott EW. Bone marrow cells adopt the phenotype of other cells by spontaneous cell fusion. Nature. 2002; 416: 542–545.[CrossRef][Medline] [Order article via Infotrieve]
  43. Kashiwakura Y, Katoh Y, Tamayose K, Konishi H, Takaya N, Yuhara S, Yamada M, Sugimoto K, Daida H. Isolation of bone marrow stromal cell-derived smooth muscle cells by a human SM22alpha promoter: in vitro differentiation of putative smooth muscle progenitor cells of bone marrow. Circulation. 2003; 107: 2078–2081.[Abstract/Free Full Text]
  44. Matsumura G, Miyagawa-Tomita S, Shin’oka T, Ikada Y, Kurosawa H. First evidence that bone marrow cells contribute to the construction of tissue-engineered vascular autografts in vivo. Circulation. 2003; 108: 1729–1734.[Abstract/Free Full Text]
  45. Babaev VR, Bobryshev YV, Stenina OV, Tararak EM, Gabbiani G. Heterogeneity of smooth muscle cells in atheromatous plaque of human aorta. Am J Pathol. 1990; 136: 1031–1042.[Abstract]
  46. Martin GM, Ogburn CE, Wight TN. Comparative rates of decline in the primary cloning efficiencies of smooth muscle cells from the aging thoracic aorta of two murine species of contrasting maximum life span potentials. Am J Pathol. 1983; 110: 236–245.[Abstract]
  47. Chamley JH, Campbell GR, Burnstock G. Dedifferentiation, redifferentiation and bundle formation of smooth muscle cells in tissue culture: the influence of cell number and nerve fibres. J Embryol Exp Morphol. 1974; 32: 297–323.[Medline] [Order article via Infotrieve]
  48. Kasai T, Pollak OJ. Smooth muscle cells in aortic cultures of untreated and cholesterol-fed rabbits. Z Zellforsch Mikrosk Anat. 1964; 62: 743–752.[CrossRef][Medline] [Order article via Infotrieve]
  49. Fritz KE, Jarmolych J, Daoud AS. Association of DNA synthesis and apparent dedifferentiation of aortic smooth muscle cells in vitro. Exp Mol Pathol. 1970; 12: 354–362.[CrossRef][Medline] [Order article via Infotrieve]
  50. Wissler RW, Vesselinovitch D. Comparative pathogenetic patterns in atherosclerosis. Adv Lipid Res. 1968; 6: 181–206.[Medline] [Order article via Infotrieve]
  51. Schor AM, Allen TD, Canfield AE, Sloan P, Schor SL. Pericytes derived from the retinal microvasculature undergo calcification in vitro. J Cell Sci. 1990; 97: 449–461.[Abstract/Free Full Text]
  52. Watson KE, Bostrom K, Ravindranath R, Lam T, Norton B, Demer LL. TGF-beta 1 and 25-hydroxycholesterol stimulate osteoblast-like vascular cells to calcify. J Clin Invest. 1994; 93: 2106–2113.[Medline] [Order article via Infotrieve]
  53. Canfield AE, Sutton AB, Hoyland JA, Schor AM. Association of thrombospondin-1 with osteogenic differentiation of retinal pericytes in vitro. J Cell Sci. 1996; 109: 343–353.[Abstract]
  54. Tintut Y, Parhami F, Bostrom K, Jackson SM, Demer LL. cAMP stimulates osteoblast-like differentiation of calcifying vascular cells. Potential signaling pathway for vascular calcification. J Biol Chem. 1998; 273: 7547–7553.[Abstract/Free Full Text]
  55. Wada T, McKee MD, Steitz S, Giachelli CM. Calcification of vascular smooth muscle cell cultures: inhibition by osteopontin. Circ Res. 1999; 84: 166–178.[Abstract/Free Full Text]
  56. Jono S, Nishizawa Y, Shioi A, Morii H. Parathyroid hormone-related peptide as a local regulator of vascular calcification. Its inhibitory action on in vitro calcification by bovine vascular smooth muscle cells. Arterioscler Thromb Vasc Biol. 1997; 17: 1135–1142.[Abstract/Free Full Text]
  57. Proudfoot D, Skepper JN, Shanahan CM, Weissberg PL. Calcification of human vascular cells in vitro is correlated with high levels of matrix Gla protein and low levels of osteopontin expression. Arterioscler Thromb Vasc Biol. 1998; 18: 379–388.[Abstract/Free Full Text]
  58. Shioi A, Nishizawa Y, Jono S, Koyama H, Hosoi M, Morii H. Beta-glycerophosphate accelerates calcification in cultured bovine vascular smooth muscle cells. Arterioscler Thromb Vasc Biol. 1995; 15: 2003–2009.[Abstract/Free Full Text]
  59. Lian JB, Stein GS. Concepts of osteoblast growth and differentiation: basis for modulation of bone cell development and tissue formation. Crit Rev Oral Biol Med. 1992; 3: 269–305.[Abstract/Free Full Text]
  60. Mohler ER III, Chawla MK, Chang AW, Vyavahare N, Levy RJ, Graham L, Gannon FH. Identification and characterization of calcifying valve cells from human and canine aortic valves. J Heart Valve Dis. 1999; 8: 254–260.[Medline] [Order article via Infotrieve]
  61. Rajamannan NM, Subramaniam M, Rickard D, Stock SR, Donovan J, Springett M, Orszulak T, Fullerton DA, Tajik AJ, Bonow RO, Spelsberg T. Human aortic valve calcification is associated with an osteoblast phenotype. Circulation. 2003; 107: 2181–2184.[Abstract/Free Full Text]
  62. Jarvelainen HT, Kinsella MG, Wight TN, Sandell LJ. Differential expression of small chondroitin/dermatan sulfate proteoglycans, PG-I/biglycan and PG-II/decorin, by vascular smooth muscle and endothelial cells in culture. J Biol Chem. 1991; 266: 23274–23281.[Abstract/Free Full Text]
  63. Shanahan CM, Cary NR, Metcalfe JC, Weissberg PL. High expression of genes for calcification-regulating proteins in human atherosclerotic plaques. J Clin Invest. 1994; 93: 2393–2402.[Medline] [Order article via Infotrieve]
  64. Doherty MJ, Ashton BA, Walsh S, Beresford JN, Grant ME, Canfield AE. Vascular pericytes express osteogenic potential in vitro and in vivo. J Bone Miner Res. 1998; 13: 828–838.[CrossRef][Medline] [Order article via Infotrieve]
  65. Farrington-Rock C, Crofts NJ, Doherty MJ, Ashton BA, Griffin-Jones C, Canfield AE. Chondrogenc and adipogenic potential of microvascular pericytes. Circulation. In press.
  66. Bostrom K, Watson KE, Horn S, Wortham C, Herman IM, Demer LL. Bone morphogenetic protein expression in human atherosclerotic lesions. J Clin Invest. 1993; 91: 1800–1809.[Medline] [Order article via Infotrieve]
  67. Romanov YA, Svintsitskaya VA, Smirnov VN. Searching for alternative sources of postnatal human mesenchymal stem cells: candidate MSC-like cells from umbilical cord. Stem Cells. 2003; 21: 105–110.[Abstract/Free Full Text]
  68. Andreeva ER, Pugach IM, Gordon D, Orekhov AN. Continuous subendothelial network formed by pericyte-like cells in human vascular bed. Tissue Cell. 1998; 30: 127–135.[CrossRef][Medline] [Order article via Infotrieve]
  69. Ahrens M, Ankenbauer T, Schroder D, Hollnagel A, Mayer H, Gross G. Expression of human bone morphogenetic proteins-2 or -4 in murine mesenchymal progenitor C3H10T1/2 cells induces differentiation into distinct mesenchymal cell lineages. DNA Cell Biol. 1993; 12: 871–880.[Medline] [Order article via Infotrieve]
  70. Ghosh-Choudhury N, Choudhury GG, Harris MA, Wozney J, Mundy GR, Abboud SL, Harris SE. Autoregulation of mouse BMP-2 gene transcription is directed by the proximal promoter element. Biochem Biophys Res Commun. 2001; 286: 101–108.[CrossRef][Medline] [Order article via Infotrieve]
  71. Garfinkel A, Tintut Y, Petrasek D, Bostrom K, Demer LL. Pattern formation by vascular mesenchymal cells. Proc Natl Acad Sci U S A. 2004; 101: 9247–9250.[Abstract/Free Full Text]
  72. Garcia-Castro MI, Marcelle C, Bronner-Fraser M. Ectodermal Wnt function as a neural crest inducer. Science. 2002; 297: 848–851.[Abstract/Free Full Text]
  73. Roskelley CD, Bissell MJ. Dynamic reciprocity revisited: a continuous, bidirectional flow of information between cells and the extracellular matrix regulates mammary epithelial cell function. Biochem Cell Biol. 1995; 73: 391–397.[Medline] [Order article via Infotrieve]
  74. Keren G, Douek P, Oblon C, Bonner RF, Pichard AD, Leon MB. Atherosclerotic saphenous vein grafts treated with different interventional procedures assessed by intravascular ultrasound. Am Heart J. 1992; 124: 198–206.[CrossRef][Medline] [Order article via Infotrieve]
  75. Lardenoye JH, de Vries MR, Lowik CW, Xu Q, Dhore CR, Cleutjens JP, van Hinsbergh VW, van Bockel JH, Quax PH. Accelerated atherosclerosis and calcification in vein grafts: a study in APOE*3 Leiden transgenic mice. Circ Res. 2002; 91: 577–584.[Abstract/Free Full Text]
  76. Caplice NM, Bunch TJ, Stalboerger PG, Wang S, Simper D, Miller DV, Russell SJ, Litzow MR, Edwards WD. Smooth muscle cells in human coronary atherosclerosis can originate from cells administered at marrow transplantation. Proc Natl Acad Sci U S A. 2003; 100: 4754–4759.[Abstract/Free Full Text]
  77. Rauscher FM, Goldschmidt-Clermont PJ, Davis BH, Wang T, Gregg D, Ramaswami P, Pippen AM, Annex BH, Dong C, Taylor DA. Aging, progenitor cell exhaustion, and atherosclerosis. Circulation. 2003; 108: 457–463.[Abstract/Free Full Text]
  78. Han CI, Campbell GR, Campbell JH. Circulating bone marrow cells can contribute to neointimal formation. J Vasc Res. 2001; 38: 113–119.[CrossRef][Medline] [Order article via Infotrieve]
  79. Shimizu K, Sugiyama S, Aikawa M, Fukumoto Y, Rabkin E, Libby P, Mitchell RN. Host bone-marrow cells are a source of donor intimal smooth- muscle-like cells in murine aortic transplant arteriopathy. Nat Med. 2001; 7: 738–741.[CrossRef][Medline] [Order article via Infotrieve]
  80. Xu Q, Zhang Z, Davison F, Hu Y. Circulating progenitor cells regenerate endothelium of vein graft atherosclerosis, which is diminished in ApoE-deficient mice. Circ Res. 2003; 93: e76–86.[Medline] [Order article via Infotrieve]
  81. Atkinson C, Horsley J, Rhind-Tutt S, Charman S, Phillpotts CJ, Wallwork J, Goddard MJ. Neointimal smooth muscle cells in human cardiac allograft coronary artery vasculopathy are of donor origin. J Heart Lung Transplant. 2004; 23: 427–435.[CrossRef][Medline] [Order article via Infotrieve]
  82. Ziegelhoeffer T, Fernandez B, Kostin S, Heil M, Voswinckel R, Helisch A, Schaper W. Bone marrow-derived cells do not incorporate into the adult growing vasculature. Circ Res. 2004; 94: 230–238.[Abstract/Free Full Text]
  83. Voswinckel R, Ziegelhoeffer T, Heil M, Kostin S, Breier G, Mehling T, Haberberger R, Clauss M, Gaumann A, Schaper W, Seeger W. Circulating vascular progenitor cells do not contribute to compensatory lung growth. Circ Res. 2003; 93: 372–379.[Abstract/Free Full Text]
  84. Tanaka K, Sata M, Hirata Y, Nagai R. Diverse contribution of bone marrow cells to neointimal hyperplasia after mechanical vascular injuries. Circ Res. 2003; 93: 783–790.[Abstract/Free Full Text]
  85. Campbell JH, Efendy JL, Campbell GR. Novel vascular graft grown within recipient’s own peritoneal cavity. Circ Res. 1999; 85: 1173–1178.[Abstract/Free Full Text]
  86. Kouchi Y, Onuki Y, Wu MH, Shi Q, Ghali R, Wechezak AR, Kaplan S, Walker M, Sauvage LR. Apparent blood stream origin of endothelial and smooth muscle cells in the neointima of long, impervious carotid-femoral grafts in the dog. Ann Vasc Surg. 1998; 12: 46–54.[CrossRef][Medline] [Order article via Infotrieve]
  87. Montfort MJ, Olivares CR, Mulcahy JM, Fleming WH. Adult blood vessels restore host hematopoiesis following lethal irradiation. Exp Hematol. 2002; 30: 950–956.[CrossRef][Medline] [Order article via Infotrieve]
  88. Simper D, Stalboerger PG, Panetta CJ, Wang S, Caplice NM. Smooth muscle progenitor cells in human blood. Circulation. 2002; 106: 1199–1204.[Abstract/Free Full Text]
  89. Gulati R, Jevremovic D, Peterson TE, Witt TA, Kleppe LS, Mueske CS, Lerman A, Vile RG, Simari RD. Autologous culture-modified mononuclear cells confer vascular protection after arterial injury. Circulation. 2003; 108: 1520–1526.[Abstract/Free Full Text]
  90. Kawamoto A, Gwon HC, Iwaguro H, Yamaguchi JI, Uchida S, Masuda H, Silver M, Ma H, Kearney M, Isner JM, Asahara T. Therapeutic potential of ex vivo expanded endothelial progenitor cells for myocardial ischemia. Circulation. 2001; 103: 634–637.[Abstract/Free Full Text]
  91. Griese DP, Ehsan A, Melo LG, Kong D, Zhang L, Mann MJ, Pratt RE, Mulligan RC, Dzau VJ. Isolation and transplantation of autologous circulating endothelial cells into denuded vessels and prosthetic grafts: implications for cell-based vascular therapy. Circulation. 2003; 108: 2710–2715.[Abstract/Free Full Text]
  92. Majka SM, Jackson KA, Kienstra KA, Majesky MW, Goodell MA, Hirschi KK. Distinct progenitor populations in skeletal muscle are bone marrow derived and exhibit different cell fates during vascular regeneration. J Clin Invest. 2003; 111: 71–79.[CrossRef][Medline] [Order article via Infotrieve]
  93. Werner N, Priller J, Laufs U, Endres M, Bohm M, Dirnagl U, Nickenig G. Bone marrow-derived progenitor cells modulate vascular reendothelialization and neointimal formation: effect of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibition. Arterioscler Thromb Vasc Biol. 2002; 22: 1567–1572.[Abstract/Free Full Text]
  94. Strehlow K, Werner N, Berweiler J, Link A, Dirnagl U, Priller J, Laufs K, Ghaeni L, Milosevic M, Bohm M, Nickenig G. Estrogen increases bone marrow-derived endothelial progenitor cell production and diminishes neointima formation. Circulation. 2003; 107: 3059–3065.[Abstract/Free Full Text]
  95. Bahlmann FH, De Groot K, Spandau JM, Landry AL, Hertel B, Duckert T, Boehm SM, Menne J, Haller H, Fliser D. Erythropoietin regulates endothelial progenitor cells. Blood. 2004; 103: 921–926.[Abstract/Free Full Text]
  96. Hill JM, Zalos G, Halcox JP, Schenke WH, Waclawiw MA, Quyyumi AA, Finkel T. Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N Engl J Med. 2003; 348: 593–600.[Abstract/Free Full Text]
  97. Laufs U, Werner N, Link A, Endres M, Wassmann S, Jurgens K, Miche E, Bohm M, Nickenig G. Physical training increases endothelial progenitor cells, inhibits neointima formation, and enhances angiogenesis. Circulation. 2004; 109: 220–226.[Abstract/Free Full Text]
  98. Beerepoot LV, Mehra N, Vermaat JS, Zonnenberg BA, Gebbink MF, Voest EE. Increased levels of viable circulating endothelial cells are an indicator of progressive disease in cancer patients. Ann Oncol. 2004; 15: 139–145.[Abstract/Free Full Text]
  99. Ramasesh N, Adams LB, Franzblau SG, Krahenbuhl JL. Effects of activated macrophages on Mycobacterium leprae. Infect Immun. 1991; 59: 2864–2869.[Abstract/Free Full Text]
  100. Darrah PA, Hondalus MK, Chen Q, Ischiropoulos H, Mosser DM. Cooperation between reactive oxygen and nitrogen intermediates in killing of Rhodococcus equi by activated macrophages. Infect Immun. 2000; 68: 3587–3593.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 J Am Coll CardiolHome page
M. Gossl, U. I. Modder, E. J. Atkinson, A. Lerman, and S. Khosla
Osteocalcin Expression by Circulating Endothelial Progenitor Cells in Patients With Coronary Atherosclerosis
J. Am. Coll. Cardiol., October 14, 2008; 52(16): 1314 - 1325.
[Abstract] [Full Text] [PDF]

Home page
 Stem CellsHome page
L. da Silva Meirelles, A. I. Caplan, and N. B. Nardi
In Search of the In Vivo Identity of Mesenchymal Stem Cells
Stem Cells, September 1, 2008; 26(9): 2287 - 2299.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
Q. Xu
Stem Cells and Transplant Arteriosclerosis
Circ. Res., May 9, 2008; 102(9): 1011 - 1024.
[Abstract] [Full Text] [PDF]

Home page
 Card Surg AdultHome page
J. E. Mayer
Tissue Engineering for Cardiac Valve Surgery
Card. Surg. Adult, January 1, 2008; 3(2008): 1649 - 1656.
[Full Text]

Home page
 Circ. Res.Home page
J. P. Kirton, N. J. Crofts, S. J. George, K. Brennan, and A. E. Canfield
Wnt/{beta}-Catenin Signaling Stimulates Chondrogenic and Inhibits Adipogenic Differentiation of Pericytes: Potential Relevance to Vascular Disease?
Circ. Res., September 14, 2007; 101(6): 581 - 589.
[Abstract] [Full Text] [PDF]

Home page
 Stem CellsHome page
G. Pasquinelli, P. L. Tazzari, C. Vaselli, L. Foroni, M. Buzzi, G. Storci, F. Alviano, F. Ricci, M. Bonafe, C. Orrico, et al.
Thoracic Aortas from Multiorgan Donors Are Suitable for Obtaining Resident Angiogenic Mesenchymal Stromal Cells
Stem Cells, July 1, 2007; 25(7): 1627 - 1634.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Neuroradiol.Home page
D. Dai, Y.H. Ding, R. Kadirvel, D.A. Lewis, H.J. Cloft, and D.F. Kallmes
Bone Formation in Elastase-Induced Rabbit Aneurysms Embolized with Platinum Coils: Report of 2 Cases
AJNR Am. J. Neuroradiol., June 1, 2007; 28(6): 1176 - 1178.
[Abstract] [Full Text] [PDF]

Home page
 Stem CellsHome page
G. Ishii, T.-K. Ito, K. Aoyagi, H. Fujimoto, H. Chiba, T. Hasebe, S. Fujii, K. Nagai, H. Sasaki, and A. Ochiai
Presence of Human Circulating Progenitor Cells for Cancer Stromal Fibro