Gaq／11和PDGF依赖性信号转导通路在大鼠主动脉再狭窄中的作用

采用大鼠主动脉球囊内皮剥脱术制备主动脉狭窄模型，观察Gop/11和GDGF信号转导通路在大鼠主动脉球囊损伤后狭窄时血管平滑肌细胞（VSMC）增殖和迁移中的作用，实验分假手术组，损伤1d组和损伤14d组，观察形态学变化，检测血管紧张素转换酶（ACE）活性和主动脉磷脂酶C（PLC）活性，用免疫印迹法测定主动脉血小板源生长因子（PDGF）受体β和Gaq/11蛋白含量，结果显示，损伤1d，主动脉内皮完全剥脱，VSMC无明显增殖和迁移，内膜无增厚，与假手术组比较，ACE 性增加382．7％（P＜0．01），PDGE受体β表达和PLC活性无明显变化，Gaq/11蛋白含量下降20．0％（P＜0．05），损伤14d组，主动脉局部有新生内皮出现，中层VSMC大量增殖并向内膜下选移，内膜显著增厚，ACE活性，PDGF受体β表达和PLC活性分别较假手术组升高420．2％（P＜0．01），85．0％（P＜0．05）和186．2％（P＜0．05），Gaq/11蛋白下降33．1％（P＜0．01）,结果提示，PDGF介导的信号转导通路可能是再狭窄时VSMC增殖的重要信号转导机制。

Roles of Galphaq/11 mediated- and platelet-derived growth factor mediated-signal transduction pathways in rat aorta restenosis

To observe the roles of Galphaq/11 mediated- and platelet-derived growth factor (PDGF) mediated-signal transduction pathways in proliferation and migration of vascular smooth muscle cells (VSMC) after arterial injury, a vascular cell proliferation model was established by balloon injury in rat aorta and the morphologic changes in injured vascular walls after the injury were studied. Activities of angiotensin converting enzyme (ACE) and aorta phospholipase C (PLC) were tested, and levels of platelet-derived growth factor receptor-beta (PDGFR-beta) and Galphaq/11 protein were measured by Western blot analysis. At l day after operation, injured aortic segments showed denudation in endothelial cells. Medial VSMC proliferation and intimal hyperplasia were not observed. As compared with the sham group, ACE activities were increased by 382.7 percent; (P<0.0l), but the expression of PDGFR-beta and PLC activities did not show significant changes (P>0.05). In addition, the level of Galphaq/11 protein was decreased by 20.0 percent; (P<0. 05). At l4 days after operation, sections of injured aorta showed marked intimal thickening with large numbers of VMSCs proliferating throughout intima and media. In comparison with the sham group, ACE activity, PLC activity and the level of PDGFR-beta were increased by 420.2 percent; (P<0.01), 186.2 percent; (P<0.05) and 85.0 percent; (P<0.05), respectively. While the level of Galphaq/11 protein was decreased by 33.1 percent; (P<0.01). The above data suggest that the PDGF-mediated signal transduction pathway plays an important role in VSMC proliferation.