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

Abstract 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 myo...

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Autores principales: Yao Gao, Yan Mei Zhang, Li Jun Qian, Ming Chu, Jian Hong, Di Xu
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/8fa29ea7c25a4ea3bdd4ce063835c63f
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spelling oai:doaj.org-article:8fa29ea7c25a4ea3bdd4ce063835c63f2021-12-02T16:07:05ZANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway10.1038/s41598-017-02585-42045-2322https://doaj.org/article/8fa29ea7c25a4ea3bdd4ce063835c63f2017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02585-4https://doaj.org/toc/2045-2322Abstract 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-β and p-smad3 declined after ANO1over-expression in cardiac fiborblasts. In conclusion, ANO1 inhibits cardiac fibrosis after MI via TGF-β/smad3 pathway in rats.Yao GaoYan Mei ZhangLi Jun QianMing ChuJian HongDi XuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Yao Gao
Yan Mei Zhang
Li Jun Qian
Ming Chu
Jian Hong
Di Xu
ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway
description Abstract 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-β and p-smad3 declined after ANO1over-expression in cardiac fiborblasts. In conclusion, ANO1 inhibits cardiac fibrosis after MI via TGF-β/smad3 pathway in rats.
format article
author Yao Gao
Yan Mei Zhang
Li Jun Qian
Ming Chu
Jian Hong
Di Xu
author_facet Yao Gao
Yan Mei Zhang
Li Jun Qian
Ming Chu
Jian Hong
Di Xu
author_sort Yao Gao
title ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway
title_short ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway
title_full ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway
title_fullStr ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway
title_full_unstemmed ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway
title_sort ano1 inhibits cardiac fibrosis after myocardial infraction via tgf-β/smad3 pathway
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/8fa29ea7c25a4ea3bdd4ce063835c63f
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