抄録
Accumulating evidence suggests that circulating progenitors potentially contribute to vascular healing and remodeling. Although there is growing enthusiasm for therapeutic and diagnostic application of circulating progenitors, there are concerns that transplanted precursors or bone marrow-derived cells may participate in the pathogenesis of unfavorable diseases. Thus, it is warranted to clarify the molecular signaling that regulates the fate of circulating vascular progenitors. We examined various vascular lesions in bone marrow (BM) chimeric mice. A significant amount of α-actin-positive cells in the vascular lesions were derived from BM. BM-derived cells also participated in re-endothelialization of the luminal side and neovascularization in the adventitia. Contribution of BM cells to neointimal hyperplasia depends on the type of injury models. Peripheral blood mononuclear cells (PBMNCs) were collected from animals or patients and cultured in the presence of various cytokines. PBMNCs differentiated into SMC-like cells or endothelial-like cells in vitro depending on the cytokines in the medium. In contrast to media-derived SMCs, the PBMNCs-derived SMC-like cells expressed abundant MMP-9 and little collagen. Coronary risk factors and angiotensin receptor blockers significantly influenced the number of circulating PBMNCs that could differentiate into SMC-like cells or endothelial-like cells. Our findings suggest that BM cells can give rise to vascular progenitor cells that home at the damaged vessels and differentiate into SMC-like cells or endothelial-like cells, thereby contributing to vascular repair, remodeling, and lesion formation. [J Physiol Sci. 2008;58 Suppl:S44]
