STAT3 Involvement in AngII-Induced Autophagy in Vascular Smooth Muscle Cells

WEI Hailiang¹, OUYANG Enhong¹, FENG Fen¹, LI Yongjie¹, LI Shuai², QIN Xuping^2*

(¹Department of Pharmacology, Shaoyang University, Shaoyang 422000, China; ²Laboratory of Vascular Biology, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421000, China)

Abstract:

This study aimed to explore the effect of STAT3 on AngII (Angiotensin II)-induced autophagy in VSMCs (vascular smooth muscle cells). The AngII-induced autophagy in VSMCs was detected after STAT3 phosphorylation inhibitor pretreatment or STAT3 gene silencing. Autophagy flow was detected by LC3 protein turnover experiment, and the expression levels of ph-STAT3(Tyr705), STAT3, LC3II, Beclin1 were detected by Western blot. The results showed that the expression of autophagy marker proteins LC3-II, Beclin1 in an AngII concentration and treatment timedependent manner. LC3-II and Beclin1 increased most significantly after VSMCs stimulated by 10–7 mol/L AngII for 24 h (P<0.05). Pretreatment of Chloroquine could further increase AngII-induced LC3-II (P<0.05). The expression levels of LC3II and Beclin1 were reversed by STAT3 phosphorylation inhibitor of Cryptotanshinone and STAT3 gene silencing (P<0.05). It is possibly that AngII promotes autophagy in VSMCs by activing STAT3 signaling pathway and AngII-induced autophagy can be reversed by STAT3 phosphorylation inhibitor or STAT3 gene silencing.

CSTR: 32200.14.cjcb.2020.12.0003