This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Sainz, J. Articles by Sata, M. Search for Related Content PubMed PubMed Citation Articles by Sainz, J. Articles by Sata, M. Related Collections Related Article

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1196.)
© 2006 American Heart Association, Inc.

Editorials

Maintenance of Vascular Homeostasis by Bone Marrow–Derived Cells

Julie Sainz; Masataka Sata

From the Departments of Cardiovascular Medicine (J.S., M.S.) and Advanced Clinical Science and Therapeutics (M.S.), University of Tokyo, Graduate School of Medicine, Japan.

Correspondence to Dr Masataka Sata, Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. E-mail msata-circ@umin.net

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The accumulation of smooth muscle cells (SMCs) plays a principal role in the pathogenesis of various vascular diseases. It has been hypothesized that dedifferentiated SMCs migrate from the media to the subendothelial space, where they proliferate and contribute to atherogenesis.¹ Similarly, it has been assumed that all of the neointimal cells in postangioplasty restenosis and graft vasculopathy are derived from adjacent medial cells. In addition to this traditional concept, recent evidence suggests that bone marrow-derived circulating precursors can also give rise to endothelial-like cells and/or smooth muscle-like cells that contribute to vascular repair, remodeling, and lesion formation in animals^2–4 and in humans.⁵ However, the contribution of bone marrow-derived cells to vascular remodeling still remains controversial.⁶ It remained to be clarified how highly "bone marrow-derived circulating progenitor cells" can differentiate into mature SMCs phenotypically and functionally.⁷

See page 1254

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Schäfer et al provide convincing evidence that bone marrow-derived cells significantly participate in neointimal formation induced by carotid arterial injury with ferric chloride (FeCl₃).⁸ Using two types of bone marrow chimeric mice, the authors found that 21% of neointimal cells and 38% of medial cells originated from the bone marrow in this mouse model of vascular injury. A significant amount of bone marrow-derived cells in the media and neointima expressed -smooth muscle actin and, to less extent, smooth muscle myosin heavy chain. Interestingly, the bone marrow-derived cells did not participate in reendothelialization as determined by double-immunostaining for von Willebrand factor (vWF) . . . [Full Text of this Article]

Related Article:

Plasminogen Activator Inhibitor-1 From Bone Marrow–Derived Cells Suppresses Neointimal Formation After Vascular Injury in Mice

Katrin Schäfer, Marco R. Schroeter, Claudia Dellas, Miriam Puls, Mirko Nitsche, Elisabeth Weiss, Gerd Hasenfuss, and Stavros V. Konstantinides
Arterioscler Thromb Vasc Biol 2006 26: 1254-1259. [Abstract] [Full Text] [PDF]