Role of the p21 cyclin-dependent kinase inhibitor in limiting intimal cell proliferation in response to arterial injury.

摘要: Arterial injury induces a series of proliferative, vasoactive, and inflammatory responses that lead to vascular proliferative diseases, including atherosclerosis restenosis. Although several factors have been defined which stimulate this process in vivo, the role specific cellular gene products limiting response is not well understood. The p21 cyclin-dependent kinase inhibitor affects cell cycle progression, senescence, differentiation transformed cells, but its expression injured blood vessels has investigated. In study, we report protein induced porcine arteries following balloon catheter suggest likely play arterial proliferation vivo. Vascular endothelial smooth muscle growth was arrested through ability inhibit progression G1 phase cycle. Following arteries, product detected neointima correlated inversely with location kinetics intimal proliferation. Direct transfer using an adenoviral vector into inhibited development hyperplasia. Taken together, these findings p21, possibly related inhibitors, may normally regulate injury, strategies increase prove therapeutically beneficial diseases.