N-acetylcysteine inhibits angiotensin II-mediated activation of extracellular signal-regulated kinase and epidermal growth factor receptor

被引:45
作者
Frank, GD
Eguchi, S
Inagami, T
Motley, ED [1 ]
机构
[1] Meharry Med Coll, Dept Anat & Physiol, Nashville, TN 37208 USA
[2] Vanderbilt Univ, Sch Med, Dept Biochem, Nashville, TN 37232 USA
关键词
angiotensin II; EGF receptor; extracellular signal-regulated kinase; N-acetylcysteine; reactive oxygen species; vascular smooth muscle cells;
D O I
10.1006/bbrc.2001.4251
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Angiotensin II (Ang II) is known to stimulate reactive oxygen species (ROS) generation and epidermal growth factor (EGF) receptor transactivation to mediate growth-promoting signals such as extracellular signal-regulated kinase (ERK) in vascular smooth muscle cells (VSMCs). However, how ROS and EGF receptor interact to orchestrate these signals in VSMCs remains unclear. Mere we found that an antioxidant, N-acetylcysteine, inhibited ERK activation and EGF receptor tyrosine phosphorylation induced by Ang II. Moreover, H2O2 stimulates EGF receptor tyrosine phosphorylation and EGF receptor inhibitors attenuated H2O2-induced ERK activation. These data indicate that ROS mediate Ang II-induced EGF receptor transactivation, a critical mechanism for ERK-dependent growth in VSMCs. (C) zool Academic Press.
引用
收藏
页码:1116 / 1119
页数:4
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