Baudouin-Legros M, Guicheney P, Meyer P
INSERM U7, Hopital Necker, Paris, France.
J Cardiovasc Pharmacol. 1990;16 Suppl 1:S1-3.
In order to define the molecular mechanism involved in enhancement of spontaneously hypertensive rat (SHR) cell proliferation, we have compared the actions of fetal calf serum (FCS) and angiotensin II on both SHR and Wistar-Kyoto (WKY) rat aortic smooth muscle cells. Both compounds are more mitogenic in SHR cells than in controls. However, phospholipase C (PLC) hyperresponsiveness can be seen only under angiotensin stimulation, as are the expressions of c-jun, c-fos, and c-myc. Oncogene overexpression therefore appears to be more strongly related to PLC hyperreactivity than to enhanced proliferation of SHR aortic smooth muscle cells.
为了确定参与自发性高血压大鼠(SHR)细胞增殖增强的分子机制,我们比较了胎牛血清(FCS)和血管紧张素II对SHR和Wistar-Kyoto(WKY)大鼠主动脉平滑肌细胞的作用。这两种化合物对SHR细胞的促有丝分裂作用均强于对照细胞。然而,只有在血管紧张素刺激下才能观察到磷脂酶C(PLC)的高反应性,c-jun、c-fos和c-myc的表达也是如此。因此,癌基因的过度表达似乎与PLC的高反应性比与SHR主动脉平滑肌细胞增殖增强的关系更为密切。