Abstract
Wild-type p53 (wt-p53), a key protein in cell cycle regulation, inactivates the G1 cyclins through direct activation of p21(Waf-1/Cip- 1/Sdi-1). Persistent vascular smooth muscle cell (VSMC) proliferation following vascular interventions hinders the benefits of these therapeutics. Using the hemagglutinating virus of Japan/liposome-mediated gene transfer method, we examined the inhibitory effect of overexpression of exogenous wt- p53 on VSMC proliferation in vitro and in vivo. We assessed the proliferative activity of human p53 cDNA-transduced bovine VSMCs by DNA synthesis assay, flow cytometry, and cell proliferation assay. p53 gene transfer reduced thymidine incorporation of VSMCs stimulated by platelet-derived growth factor-BB (P
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Yonemitsu, Y., Kaneda, Y., Tanaka, S., Nakashima, Y., Komori, K., Sugimachi, K., & Sueishi, K. (1998). Transfer of wild-type p53 gene effectively inhibits vascular smooth muscle cell proliferation in vitro and in vivo. Circulation Research, 82(2), 147–156. https://doi.org/10.1161/01.RES.82.2.147
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