Regulation of ERK5 by insulin and angiotensin-II in vascular smooth muscle cells.
Regulation of ERK5 by insulin and angiotensin-II in vascular smooth muscle cells.
复制标题
血管平滑肌细胞中胰岛素和血管紧张素 II 对 ERK5 的调节。
DOI：
10.1016/j.bbrc.2007.01.102
复制
发表时间：
2007
影响因子：
3.1
通讯作者：
Goalstone,MarcLee
中科院分区：
文献类型：
--
作者：
Sharma,Girish;Goalstone,MarcLee
ERK5参与血管平滑肌细胞(VSMC)的增殖。胰岛素和血管紧张素-II(A-II)对VSMC的增殖作用部分是通过ERK1/2介导的。我们推测胰岛素和A-II也调节VSMC中ERK5的活性。用胰岛素或A-II急性处理(60min)后，ERK1/2和ERK5的磷酸化水平在15min和5min分别增加。慢性胰岛素处理(⩽8h)可使ERK1/2磷酸化增加4h，ERK5磷酸化增加8h。A-II刺激ERK1/2磷酸化8h，ERK5磷酸化4h。胰岛素对ERK1/2和ERK5磷酸化的EC50分别为1.5和0.1nM，而对A-II的EC50分别为2 nM。胰岛素+A-II仅对ERK5的磷酸化有相加作用。PD98059和Wortmannin抑制胰岛素和A-II刺激的ERK5和ERK1/2的磷酸化表现出不同的和时间依赖的效应。综上所述，这些数据表明，胰岛素和A-II调节ERK5的活性，但不同于ERK1/2。
ERK5 is involved in proliferation of vascular smooth muscle cells (VSMC). The proliferative actions of insulin and angiotensin-II (A-II) in VSMC are mediated in part by ERK1/2. We hypothesized that insulin and A-II also regulate ERK5 activity in VSMC. Acute treatment (<60min) with insulin or A-II increased phosphorylation of ERK1/2 at 15min and ERK5 at 5min. Chronic treatment (⩽8h) with insulin increased ERK1/2 phosphorylation by 4h and ERK5 by 8h. A-II-stimulated phosphorylation of ERK1/2 by 8h and ERK5 by 4h. The EC50for insulin treatment effecting ERK1/2 and ERK5 phosphorylation was 1.5 and 0.1nM, whereas the EC50for A-II was 2nM, each. Insulin plus A-II induced an additive effect only on ERK5 phosphorylation. Inhibition of insulin- and A-II-stimulated phosphorylation of ERK5 and ERK1/2 by PD98059 and Wortmannin exhibited differential and time-dependent effects. Taken together, these data indicate that insulin and A-II regulate the activity of ERK5, but different from that seen for ERK1/2.