ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway

被引：27

作者：

Gao, Yao ^{[1
]}

Zhang, Yan Mei ^{[1
]}

Qian, Li Jun ^{[1
]}

Chu, Ming ^{[1
]}

Hong, Jian ^{[1
]}

Xu, Di ^{[1
]}

机构：

[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Geriatr, Nanjing 210029, Jiangsu, Peoples R China

来源：

SCIENTIFIC REPORTS | 2017年 / 7卷

基金：

中国国家自然科学基金;

关键词：

CA2+-ACTIVATED CL-CHANNEL; TISSUE GROWTH-FACTOR; TGF-BETA; FIBROBLAST PROLIFERATION; EXPRESSION; TMEM16A; CONTRIBUTES; ACTIVATION; INTEGRINS; PROTEIN;

D O I：

10.1038/s41598-017-02585-4

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

As a newly identified factor in calcium-activated chloride channel, ANO1 participates in various physiological processes like proliferation and differentiation, and expresses in human cardiac fibroblasts. In this experiment, we investigated the function of ANO1 in cardiac fibrosis after myocardial infraction (MI) with methods of Western blotting, Quantitative real-time PCR (qRT-PCR), metabolic reduction of 3-(4,5-dimethylthiozol-2-yl)-2, 5-diphenyltetrazo-lium bromide (MTT), immunofluorescence and confocal imaging, and Masson's trichrome staining. The results showed that the expression of ANO1 significantly increased in neonatal rats' cardiac fibroblasts after hypoxia and in cardiac tissues after MI. After ANO1 over-expression, cardiac fibrosis was reduced in vitro and in vivo. Moreover, the expression of TGF-beta and p-smad3 declined after ANO1over-expression in cardiac fiborblasts. In conclusion, ANO1 inhibits cardiac fibrosis after MI via TGF-beta/smad3 pathway in rats.

引用

页数：9

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