Experimental study of miR-26a regulating CTGF expression in radiation-induced heart disease
10.3760/cma.j.cn113030-20210615-00154
- VernacularTitle:miR-26a调控CTGF表达在放射性心脏损伤中作用的实验研究
- Author:
Rui YAN
1
;
Honghong CAI
;
Min GUO
;
Jianbo SONG
;
Xianhai XU
;
Yarong ZHANG
;
Yang YU
;
Sijin LI
Author Information
1. 山西医科大学第一医院核医学科，太原 030001
- Keywords:
MiR-26a;
Connective tissue growth factor;
Radiation induced heart disease;
Cardiac fibroblasts;
Myocardial fibrosis
- From:
Chinese Journal of Radiation Oncology
2022;31(12):1147-1152
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the regulatory effect of miR-26a in radiation-induced heart disease (RIHD) mice.Methods:C57/BL6 mice were used to establish RIHD models. The cardiac function, fibrosis, the expression levels of collagen 1 (COL1) and connective tissue growth factor (CTGF), and miR-26a were detected in RIHD mice. Whether CTGF was the target gene of miR-26a was verified by dual luciferase kit. Moreover, cardiac fibroblasts were transfected with miR-26a up and miR-26a down lentivirus vectors to construct the miR-26a overexpression and underexpression cell models. The expression of CTGF, proliferation, and apoptosis of cardiac fibroblasts were detected.Results:In the RIHD mice, heart function was decreased, myocardial fibrosis was remodeled, the expression levels of COL1 and CTGF were up-regulated, and the expression level of miR-26a was down-regulated. Dual luciferase reporter assay confirmed that CTGF was the target gene regulated by miR-26a. Overexpression of miR-26a could inhibit the expression of CTGF, suppress the proliferation of cardiac fibroblasts, promote cell apoptosis and secrete collagen. Underexpression of miR-26a yielded the opposite results.Conclusion:MiR-26a affects the function of cardiac fibroblasts by targeting CTGF and probably mediates the process of radiation-induced myocardial fibrosis, which may become a new regulatory target of RIHD.
