Baudouin-Legros M, Paquet J L, Brunelle G, Meyer P
Inserm U 7, Hôpital Necker, Paris, France.
J Hypertens Suppl. 1989 Dec;7(6):S114-5. doi: 10.1097/00004872-198900076-00053.
In order to define the molecular mechanism involved in the enhancement of spontaneously hypertensive rat (SHR) cell proliferation, we compared the actions of fetal calf serum and angiotensin II on both SHR and Wistar-Kyoto rat (WKY) aortic smooth muscle cells. Both compounds were more mitogenic on the SHR cells than on the controls. However, phospholipase C hyper-responsiveness was present only after angiotensin stimulation. This was also true of the expression of c-jun, c-fos and c-myc. Oncogene overexpression therefore appears to be more strongly related to phospholipase C 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和血管紧张素II对SHR和Wistar-Kyoto大鼠(WKY)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组。然而,仅在血管紧张素刺激后才出现磷脂酶C高反应性。c-jun、c-fos和c-myc的表达情况也是如此。因此,癌基因的过度表达似乎与磷脂酶C高反应性的关系比与SHR主动脉平滑肌细胞增殖增强的关系更为密切。