Downregulation of S100A4 Alleviates Cardiac Fibrosis via Wnt/β -Catenin Pathway in Mice

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
Li Jun QianDi Xu

Abstract

Cardiac fibrosis is a pathological change leading to cardiac remodeling during the progression of myocardial ischemic diseases, and its therapeutic strategy remains to be explored. S100A4, a calcium-binding protein, participates in fibrotic diseases with an unclear mechanism. This study aimed to investigate the role of S100A4 in cardiac fibrosis. Cardiac fibroblasts from neonatal C57BL/6 mouse hearts were isolated and cultured. Myocardial infarction was induced by ligating the left anterior descending coronary artery (LAD). The ligation was not performed in the sham group. A volume of 5×105pfu/g adenovirus or 5 µM/g ICG-001 was intramyocardially injected into five parts bordering the infarction zone or normal region. We used Western blotting, quantitative RT-PCR, immunofluorescence, immunohistochemistry and Masson's trichrome staining to explore the function of S100A4. We found significant increases of S100A4 level and cardiac fibrosis markers, and β-catenin signaling activation in vitro and in vivo. In addition, knockdown of S100A4 significantly reduced cardiac fibrosis and β-catenin levels. Moreover, the expression of S100A4 decreased after ICG-001 inhibited β-catenin signal pathway. Downregulation of S100A4 alleviates cardia...Continue Reading

Citations

Oct 5, 2018·Frontiers in Physiology·Simon BraumannFelix W Friedrich
Jun 11, 2020·Cell Communication and Signaling : CCS·Fatemeh YousefiMichael R Hamblin
Jan 27, 2021·Cells·Evangelos P Daskalopoulos, W Matthijs Blankesteijn
Nov 30, 2019·Biochimica Et Biophysica Acta. Molecular Basis of Disease·Xianxiu WanNisha J Garg
Jul 6, 2020·Biochimica Et Biophysica Acta. Molecular Cell Research·Wenqing LiuJinlian Hua

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