Section of Molecular Medicine, National Heart and Lung Institute, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, London SW7 2AZ, UK.
Biochem Biophys Res Commun. 2010 Jan 1;391(1):818-23. doi: 10.1016/j.bbrc.2009.11.145. Epub 2009 Dec 2.
Vascular smooth muscle cell (VSMC) proliferation remains a major cause of veno-arterial graft failure. We hypothesised that exposure of venous SMCs to arterial pressure would increase KLF5 expression and that of cell cycle genes. Porcine jugular veins were perfused at arterial or venous pressure in the absence of growth factors. The KLF5, c-myc, cyclin-D and cyclin-E expression were elevated within 24h of perfusion at arterial pressure but not at venous pressure. Arterial pressure also reduced the decline in SM-myosin heavy chain expression. These data suggest a role for KLF5 in initiating venous SMCs proliferation in response to arterial pressure.
血管平滑肌细胞(VSMC)增殖仍然是动静脉移植物失败的主要原因。我们假设,静脉平滑肌细胞暴露于动脉压下会增加 KLF5 的表达及其细胞周期基因的表达。在不存在生长因子的情况下,用动脉压或静脉压对猪颈静脉进行灌注。在动脉压灌注的 24 小时内,KLF5、c-myc、细胞周期蛋白 D 和 E 的表达升高,但在静脉压下没有升高。动脉压还降低了 SM-肌球蛋白重链表达的下降。这些数据表明 KLF5 在启动静脉平滑肌细胞对动脉压的增殖反应中起作用。