[Candesartan inhibits the angiotensin II-induced proliferation and migration of rat thoracic aortic smooth muscle A7r5 cells and its mechanism].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

Ministry-of-Education Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Department of Physiology, Shihezi University School of Medicine, Shihezi 832000, China. *Corresponding authors, E-mail:

Published: February 2019

Objective To investigate the effect of candesartan on angiotensin II (Ang II)-induced proliferation and migration of vascular smooth muscle cells and its effect on connexin 43 (Cx43). Methods A7r5 cells were cultured in vitro and randomly divided into control group, AngII group and AngII combined with candesartan group. Cell viability was detected by CCK-8 assay; the migration and invasion ability of A7r5 cells were measured by wound-healing and Transwell assay; the expression and distribution of Cx43 on A7r5 cells were detected by immunofluorescence assay. Cx43, osteopontin (OPN), proliferating cell nuclear antigen (PCNA), p-MEK1/2 and p-ERK1/2 protein levels of A7r5 cells were detected by Western blot analysis. Results Compared with the control group, the AngII group had higher cell proliferation and migration ability, and the AngII combined with candesartan group had a lower concentration than the AngII group. Cx43 was expressed in the A7r5 cell membrane and nuclear membrane. The expression of Cx43 were enhanced in the AngII group than in the control group, and the expressions of Cx43, OPN, PCNA, p-MEK1/2 and p-ERK1/2 significantly increased compared with AngII. The expression of protein significantly decreased in AngII combined with candesartan group. Conclusion Candesartan can reduce the proliferation and migration of smooth muscle cells induced by AngII, and its mechanism may be related to Cx43 and MEK/ERK signaling pathways.

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