期刊
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
卷 25, 期 7, 页码 1383-1387出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.ATV.0000168415.33812.51
关键词
adventitia; restenosis; balloon angioplasty; smad7; TGF-beta 1
Objective-Migration of adventitial fibroblasts contributes to arterial remodeling after angioplasty. This study used vascular gene transfer of smad7 to investigate whether antagonism of transforming growth factor-beta 1 signaling alters luminal loss and adventitial cell migration after balloon injury in rat carotid arteries. Methods and Results-Adenoviruses coordinating expression of beta-galactosidase (beta-gal) and smad7 or beta-gal and green fluorescent protein (GFP) were applied to the perivascular surface of common carotid arteries. Balloon injury was performed 4 days after gene transfer, and animals were killed at 3, 7, and 14 days after injury. Uninjured arteries only expressed adventitial beta-gal positive cells; however, after balloon injury in beta-gal- and GFP-transfected arteries, beta-gal-positive cells were observed within the medial layer of vessels and contributed to the population of cells within the neointima at 7 to 14 days. Overexpression of smad7 and beta-gal resulted in a significant reduction in the number of beta-gal-labeled cells in the neointima, concomitant with reduced luminal loss and decreased adventitial collagen content. Conclusions-We provide the first evidence that vascular smad7 overexpression attenuates remodeling and contribution of adventitial fibroblasts to neointima formation after balloon angioplasty. Smad7 may represent a novel therapeutic target to reduce the incidence of restenosis.
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