Related Experiment Video
Updated: Mar 6, 2026
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Effect of miR-203 expression on myocardial fibrosis
1Department of Cardiology, Tianjin First Center Hospital, Tianjin, China. chengzhiluasd@sina.com.
Insights
MicroRNA-203 (miR-203) inhibits myocardial fibrosis by reducing fibrosis markers like TGF-β1. Upregulating miR-203 decreases these markers, while inhibiting miR-203 increases them, suggesting miR-203
Area of Science:
- Cardiovascular biology
- Molecular cardiology
- Biochemistry
Background:
- Cardiovascular diseases pose a significant global health threat.
- Myocardial fibrosis is a primary contributor to cardiovascular disease progression.
- MicroRNA-203 (miR-203) has been identified as a potential inhibitor of fibrosis.
Purpose of the Study:
- To investigate the impact of miR-203's differential expression on fibrosis in cultured mouse cardiomyocytes.
- To explore the role of miR-203 in regulating key fibrosis-related factors.
Main Methods:
- miR-203 activators and inhibitors were designed and synthesized.
- These were transfected into mouse cardiomyocytes, establishing activator, inhibitor, and control groups.
- Expression levels of fibronectin (FN), connective tissue growth factor (CTGF), and transforming growth factor-beta 1 (TGF-β1) were quantified using Western blot and RT-PCR.
Main Results:
- Overexpression of miR-203 significantly reduced TGF-β1, CTGF, and FN expression in a time-dependent manner.
- Inhibition of miR-203 significantly increased TGF-β1, CTGF, and FN expression at 36 hours post-transfection.
- No significant changes were observed at 24 hours post-transfection for any group.
Conclusions:
- miR-203 overexpression effectively suppresses myocardial fibrosis markers (TGF-β1, CTGF, FN).
- These fibrosis markers may serve as predictive indicators for fibrosis.
- Modulating miR-203 levels offers a potential therapeutic strategy for cardiovascular diseases.
Objective:
Cardiovascular disease is one of the diseases threatening human health. Myocardial fibrosis is a major cause of cardiovascular diseases. Studies have shown that over expression of miR-203 can inhibit the fibrosis. Therefore, in this study, the effect of differential expression of miR-203 on fibrosis of cultured mouse cardiomyocytes was investigated.
Materials And Methods:
Activators and inhibitors of miR-203 were designed according to the sequence of miR-203, synthesized, and transfected into mouse cardiomyocytes to establish activator group, inhibitor group, and control group. The expression levels of fibrosis-related factors including FN, CTGF, and TGF-β1 were measured by Western blot and RT-PCR 24 h and 36 h after transfection.
Results:
Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN in a time-dependent manner, compared with that in the control group (p <0.05). Inhibition of miR-203 expression in mouse cardiomyocytes significantly increased the expression levels of TGF-β1, CTGF, and FN 36 h after transfection, compared with that in the control group (p < 0.05). No significant differences were seen in the expression levels of TGF-β1, CTGF, and FN 24 h after transfection, compared with that in the control group (p >0.05).
Conclusions:
Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN, which might be used as a detection index for prediction of fibrosis.
