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.
Highlights
Myocardial infarction(MI) is a leading cause of death worldwide[1]
We stained cardiac fibroblasts, ANO1 protein, and nucleus by immunofluorescent confocal microscopic analysis (Fig. 1D). These results demonstrated ANO1 protein existed in the cardiac fibroblasts of neonatal rats and the expression was higher than that in myocardial cells
According to western blotting analysis, compared to untreated group, the level of a-SMA at the point of 6, 8, 10, 16, and 24 hourincreased gradually after hypoxia and peaked at the point of 24 hour (Fig. 2B,C). These results demonstrated that cardiac fibroblast activated after hypoxia developed into myofibroblasts and set off cardiac fibrosis
Summary
Myocardial infarction(MI) is a leading cause of death worldwide[1]. percutaneous coronary intervention (PCI) has improved the survival, post-MI heart failure still occurs after various adverse cardiac remodeling, including cardiac fibrosis, cardiomyocyte apoptosis, inflammatory reaction, etc[2]. Exessive proliferation of fibroblasts and deposition of extracellular matrix (ECM) proteins are stimulated by cardiac fibroblasts in the myocardium[7,8,9]. In 2009, M.A.Olman announced that TGF- β/Smad[3] pathway induces myofibroblasts expression and enhances deposition of extracellular matrix proteins such as collagen I and III via Smad[3] activation[30]. Based on these findings, we propose that ANO1 takes part in the process of cardiac fibrosis via TGF-β/Smad[3] signaling pathway
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