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Maintenance of vascular homeostasis by bone marrow-derived cells.

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 animals2–4 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 , Schafer 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 …