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MiR-25-3p promotes the expression of fibrosis-related genes in cardiac fibroblasts through BTG2/SOD2 axis
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1.School of Pharmacy, Southern Medical University, Guangzhou, Guangdong 510515, China;2.School of Medicine, South China University of Technology, Guangzhou, Guangdong 510006, China;3.Guangdong Cardiovascular Institute, Guangzhou, Guangdong 510080, China;4.School of Biology and Biological Engineering, South China University of Technology, Guangzhou, Guangdong 510006, China;5.The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510280, China;6.Guangdong Provincial Key Laboratory of Clinical Pharmacology ＆ Guangdong Provincial People’s Hospital ＆ Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, China)

Clc Number:

R329.21；R5

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    Abstract:

    Aim To investigate the effect of microRNA miR-25-3p on fibrosis-related gene expression in cardiac fibroblasts and mechanism involved. Methods A mouse model of cardiac fibrosis induced by angiotensin Ⅱ (AngⅡ) infusion was constructed, and the differentially expressed miRNAs in the fibrotic mouse myocardium were detected by miRNA chip array. Primary isolation and culture of C57BL/6 mouse cardiac fibroblasts (mCF) were performed, and a cell model of myocardial fibrosis was established based on AngⅡ-treated mCF. The effect of miR-25-3p mimic on the expression of fibrosis-related genes in mCF was studied. The dual luciferase reporter gene assay was performed to verify the binding of miR-25-3p on the 3′-untranslated region (3′UTR) of the B-cell translocation gene 2 (BTG2) gene. Actinomycin D experiment was performed to detect the effect of BTG2 on the stability of superoxide dismutase 2 (SOD2) mRNA in mCF. Results Expression of miR-25-3p was increased in the myocardium of AngⅡ-infused mice and AngⅡ-treated mCF. miR-25-3p could enhance the expression of fibrosis-related genes, including collagen type Ⅰ alpha 1 chain (COL1A1), collagen type Ⅲ alpha 1 chain(COL3A1) and α-smooth muscle actin(α-SMA) in mCF. BTG2 was confirmed to be a target gene of miR-25-3p, and BTG2 mediated the effect of miR-25-3p on promoting fibrosis-related gene expression in mCF. In addition, BTG2 could enhance the expression of SOD2 by increasing the stability of SOD2 mRNA in mCF. Conclusion MiR-25-3p inhibited the level of SOD2 through targeting BTG2 in mCF, resulting in enhancing fibrosis-related gene expression and promoting myocardial fibrosis.

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ZHAO Anzhi, GUO Jing, CHEN Liwen, HUANG Zhiqi, CHEN Zerun, ZHU Jiening, ZHANG Mengzhen, ZHANG Ming, XU Jindong, SHAN Zhixin. MiR-25-3p promotes the expression of fibrosis-related genes in cardiac fibroblasts through BTG2/SOD2 axis[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2022,30(4):328-334, 351.

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History
  • Received:August 21,2021
  • Revised:November 17,2021
  • Online: March 31,2022
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