Bone marrow-derived vascular cells in response to injury.

Intimal hyperplasia is a key lesion for various vascular disorders such as atherosclerosis, postangioplasty restenosis and transplant arteriopathy. It has widely been accepted that intimal smooth muscle cells (SMC) originate from the medial layer in the same artery. However, recent studies suggest that bone marrow can also provide circulating progenitors for vascular SMC. Bone marrow-derived SMC participate in neointimal formation in animal models of allotransplantation, severe mechanical injury and hyperlipidemia-induced atherosclerosis. In human, transplantation arteriopathy also seems to involve circulating SMC, but their role in atherosclerosis and restenosis remains to be elucidated. Mobilization, differentiation and proliferation steps of SMC progenitors will provide promising targets for novel therapeutic approaches against proliferative vascular diseases.

[1]  D. Hullett Smooth Muscle Progenitor Cells of Bone Marrow Origin Contribute to the Development of Neointimal Thickenings in Rat Aortic Allografts and Injured Rat Carotid Arteries , 2002 .

[2]  Qingbo Xu,et al.  Both Donor and Recipient Origins of Smooth Muscle Cells in Vein Graft Atherosclerotic Lesions , 2002, Circulation research.

[3]  Qingbo Xu,et al.  Smooth Muscle Cells in Transplant Atherosclerotic Lesions Are Originated From Recipients, but Not Bone Marrow Progenitor Cells , 2002, Circulation.

[4]  G. Spangrude,et al.  Chimerism of the transplanted heart. , 2002, The New England journal of medicine.

[5]  E. Scott,et al.  Bone marrow cells adopt the phenotype of other cells by spontaneous cell fusion , 2002, Nature.

[6]  M. Makuuchi,et al.  Hematopoietic stem cells differentiate into vascular cells that participate in the pathogenesis of atherosclerosis , 2002, Nature Medicine.

[7]  P. Nickerson,et al.  Neointimal and tubulointerstitial infiltration by recipient mesenchymal cells in chronic renal-allograft rejection. , 2001, The New England journal of medicine.

[8]  G. Williams,et al.  Vascular smooth muscle cells of recipient origin mediate intimal expansion after aortic allotransplantation in mice. , 2001, The American journal of pathology.

[9]  P. Libby,et al.  Host bone-marrow cells are a source of donor intimal smooth- muscle–like cells in murine aortic transplant arteriopathy , 2001, Nature Medicine.

[10]  Julie H. Campbell,et al.  Circulating Bone Marrow Cells Can Contribute to Neointimal Formation , 2001, Journal of Vascular Research.

[11]  K. Williams,et al.  Atherosclerosis--an inflammatory disease. , 1999, The New England journal of medicine.

[12]  Takayuki Asahara,et al.  Isolation of Putative Progenitor Endothelial Cells for Angiogenesis , 1997, Science.

[13]  A. Zalewski,et al.  Adventitial myofibroblasts contribute to neointimal formation in injured porcine coronary arteries. , 1996, Circulation.

[14]  J. Wilcox,et al.  Identification of a potential role for the adventitia in vascular lesion formation after balloon overstretch injury of porcine coronary arteries. , 1996, Circulation.

[15]  R. Ross The pathogenesis of atherosclerosis: a perspective for the 1990s , 1993, Nature.

[16]  Julie H. Campbell,et al.  The Phenotypes of Smooth Muscle Expressed in Human Atheroma a , 1990, Annals of the New York Academy of Sciences.

[17]  H. Mabuchi,et al.  Effect of pravastatin-induced LDL-cholesterol reduction on coronary heart disease and cerebrovascular disease in Japanese: Hokuriku lipid coronary heart disease study-pravastatin atherosclerosis trial (Holicos-PAT). , 2002, Journal of atherosclerosis and thrombosis.

[18]  M. Makuuchi,et al.  Circulating smooth muscle progenitor cells contribute to atherosclerosis , 2001, Nature Medicine.