Ding X L, Zhou C Y, Li Y X
Laboratory of Cardiovascular Physiology, Human Medical University, Changsha.
Sheng Li Xue Bao. 1994 Oct;46(5):465-72.
In order to study the roles of protein kinase C (PKC) and Na(+)-H+ exchange in [Sar1] ANG II-induced hypertrophic response, 3H-Leucine incorporation into serum-free cultured neonatal rat cardiomyocytes were interfered with staurosporine, phorbol 12-myristate 13-acetate (PMA) or amiloride. With [Sar1] ANG II, a dose dependent augmentation of protein synthesis was observed. Activator of PKC (PMA) could also accelerate the rate of protein synthesis to a significant extent, while pretreatment of cardiac myocytes with PKC inhibitor (staurosporine) or Na(+)-H+ exchanger inhibitor (amiloride) would block [Sar1] ANG II-induced increase 3H-Leucine incorporation. These results demonstrated that activation of PKC and Na(+)-H+ exchange might mediate the hypertrophic response initiated by [Sar1] ANG II. However, inhibition of cellular Na(+)-H+ exchange did not affect the increase in protein synthesis due to activation of PKC, a finding indicating that the two resorts to regulate cell growth are mediated by independent pathways.
为研究蛋白激酶C（PKC）和Na(+)-H+交换在[Sar1]血管紧张素II诱导的肥大反应中的作用，用星形孢菌素、佛波酯12-肉豆蔻酸酯13-乙酸酯（PMA）或阿米洛利干扰无血清培养新生大鼠心肌细胞中3H-亮氨酸的掺入。给予[Sar1]血管紧张素II后，观察到蛋白质合成呈剂量依赖性增加。PKC激活剂（PMA）也能在很大程度上加速蛋白质合成速率，而用PKC抑制剂（星形孢菌素）或Na(+)-H+交换抑制剂（阿米洛利）预处理心肌细胞会阻断[Sar1]血管紧张素II诱导的3H-亮氨酸掺入增加。这些结果表明，PKC的激活和Na(+)-H+交换可能介导了由[Sar1]血管紧张素II引发的肥大反应。然而，抑制细胞Na(+)-H+交换并不影响因PKC激活导致的蛋白质合成增加，这一发现表明这两种调节细胞生长的途径是由独立的信号通路介导的。
