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MiR-29a regulates cardiomyocyte apoptosis by targeting Bak1 in diabetic cardiomyopathy
Xiaoyan Wang1,2, Zhitao Zhang3, Mei Wang1
1Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050004, China.
Abstract:
This study sought to investigate the association between microRNA-29a (miR-29a) and cardiomyocyte apoptosis in diabetic cardiomyopathy (DCM). DCM rat model was established by treating rats with streptozotocin (STZ), followed by injection of NC or miR-29a-3p mimics into the myocardium of rats. High glucose (HG)-treated H9c2 cells were transfected with NC and miR-29a-3p mimics. DCM rats presented elevated levels of blood glucose, HbA1c, blood pressure, urine output, decreased body weight and cardiac contractile function after modeling. MiR-29a was lowly expressed in STZ-treated rats and HG-treated H9c2 cells. Upregulation of miR-29a improved cardiac structure and function and attenuated, alleviated myocardial histological abnormalities and fibrosis and lowered cardiomyocyte apoptosis in DCM rats. Meanwhile, HG promoted H9c2 cell apoptosis, while miR-29a overexpression attenuated the function of HG. Compared with control group, the protein expression of Bax, cleaved-caspase3 and Bak1 in DCM and HG groups were significantly upregulated, and the expression of Bcl-2 and Mcl-1 was downregulated, while miR-29a overexpression exerted opposite effect. Bioinformatics prediction method and western blot revealed that miR-29a directly targeted Bak1 and downregulated Bak1 expression. Overall, miR-29a regulated STZ- and HG-induced cardiomyocyte apoptosis by targeting Bak1, providing a novel understanding of the pathogenesis of DCM.
Insights
MicroRNA-29a (miR-29a) protects against diabetic cardiomyopathy (DCM) by reducing cardiomyocyte apoptosis. Upregulating miR-29a in DCM models improved heart function and targeted Bak1, offering new insights into DCM's development.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Diabetic cardiomyopathy (DCM) is a significant complication of diabetes, characterized by cardiac dysfunction.
- The role of microRNAs in the pathogenesis of DCM is an area of active research.
- Cardiomyocyte apoptosis contributes to the progression of DCM.
Purpose of the Study:
- To investigate the association between microRNA-29a (miR-29a) and cardiomyocyte apoptosis in a diabetic cardiomyopathy (DCM) model.
- To elucidate the mechanism by which miR-29a influences DCM pathogenesis.
Main Methods:
- Established a DCM rat model using streptozotocin (STZ) and high glucose (HG)-treated H9c2 cells.
- Administered miR-29a mimics to DCM rats and transfected H9c2 cells with miR-29a mimics.
- Assessed cardiac function, histological abnormalities, apoptosis markers, and protein expression (Bax, Bcl-2, Bak1, Mcl-1, cleaved-caspase3).
- Utilized bioinformatics and Western blot to identify miR-29a targets.
Main Results:
- STZ-induced DCM rats and HG-treated cells exhibited reduced miR-29a expression.
- miR-29a upregulation improved cardiac structure and function, attenuated fibrosis, and reduced cardiomyocyte apoptosis in DCM rats.
- miR-29a overexpression counteracted the pro-apoptotic effects of HG in H9c2 cells.
- miR-29a directly targeted and downregulated Bak1 expression, while altering the expression of other apoptosis-related proteins (Bax, Bcl-2, Mcl-1, cleaved-caspase3).
Conclusions:
- miR-29a plays a protective role in DCM by inhibiting cardiomyocyte apoptosis.
- miR-29a targets Bak1, providing a novel mechanism for its cardioprotective effects in DCM.
- These findings offer new insights into the pathogenesis of DCM and suggest miR-29a as a potential therapeutic target.
