Upregulation of sestrin-2 expression protects against endothelial toxicity of angiotensin II

• DOI: 10.1007/s10565-014-9276-3
• Publication Date: 2014-05-17T06:43:50Z
• Authors: Lao Yi; Feng Li; Yuan Yong; Dong Jianting; Zhang Liting; Huang Xuansheng; Li Fei; Li Jiewen
• Keywords: c-jun

Sestrin-2 (SESN2) is involved in the cellular response to different stress conditions. However, function of SESN2 cardiovascular system remains unknown. In present study, we tested whether has a beneficial effect on vascular endothelial damage induced by angiotensin II (AngII). Firstly, found that AngII induces expression human umbilical vein cells (HUVECs) time-dependent and dose-dependent manner. We also knockdown using small RNA interference promotes toxicity AngII, as well reduction cell viability, exacerbation oxidative stress, stimulation apoptosis. addition, our results show c-Jun NH (2)-terminal kinase (JNK)/c-Jun pathway activated AngII. Inhibiting activity JNK abolishes increase Importantly, overexpression luciferase promoter. These findings suggest inductive mediated JNK/c-Jun pathway. Our indicate induction acts compensatory for survival, implying stimulating might be an effective pharmacological target treatment AngII-associated diseases.