Scott-Burden T, Resink T J, Baur U, Bürgin M, Bühler F R
Department of Research, University Hospital, Basel, Switzerland.
Biochem Biophys Res Commun. 1988 Feb 29;151(1):583-9. doi: 10.1016/0006-291x(88)90634-1.
Angiotensin II was shown to activate S6-kinase in cultured vascular smooth muscle cells (VSMC) in a dose- (10(-9)-10(-6) M) and time-dependent manner. Pretreatment of quiescent cells with 12-O-Tetradecanoylphorbol-13-acetate had no effect on the activation levels of the kinase at the hormone levels used. However, stimulation of S6-kinase activity by angiotensin II was markedly inhibited by the inclusion of amiloride hydrochloride in serum-free medium during activation procedures. Angiotensin was not mitogenic for VSMC at even the highest doses used (10(-6) M). These findings support the notion that raised intracellular pH results in the activation of protein synthesis in quiescent cells.
血管紧张素II在培养的血管平滑肌细胞(VSMC)中呈剂量(10^(-9)-10^(-6)M)和时间依赖性激活S6激酶。用12-O-十四烷酰佛波醇-13-乙酸酯预处理静止细胞,在所使用的激素水平下对激酶的激活水平没有影响。然而,在激活过程中,无血清培养基中加入盐酸阿米洛利可显著抑制血管紧张素II对S6激酶活性的刺激。即使使用最高剂量(10^(-6)M),血管紧张素对VSMC也没有促有丝分裂作用。这些发现支持细胞内pH升高导致静止细胞中蛋白质合成激活的观点。