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STAT4 regulates cardiomyocyte apoptosis in rat models of diabetic cardiomyopathy
Mei He1, Ming Li2, ZhiKun Guo1
1Henan Medical Key Laboratory of Arrhyrithmia, Zhengzhou No. 7 People's Hospital, Zhengzhou 450016, China.
Objective:
This study aimed to investigate the protective role of the signal transducer and activator of transcription 4 (STAT4) in diabetic cardiomyopathy.
Materials And Methods:
Male Sprague-Dawley (SD) rats (6-8 weeks old) were purchased from the Experimental Animal Center of Zhengzhou University. The rats were randomly divided into the control and diabetic cardiomyopathy groups. Rat models of diabetic cardiomyopathy were established by a high-sugar and high-fat diet combined with a peritoneal injection of streptozocin. Pathological changes in the heart were visualized using Hematoxylin-eosin (HE) staining and Masson's staining. Moreover, cell apoptosis was detected using terminal deoxyribonucleotidyl transferase (TdT)-mediated biotin-16-dUTP nick-end labeling (TUNEL) staining and Annexin V apoptosis detection kit. Furthermore, H9C2 cells were transfected with lentivirus overexpressing STAT4 and treated with high glucose. The CCK-8 assay was performed to determine cell viability. Finally, Western blotting was used to determine the expression of STAT4, Bax, and Bcl-2.
Results:
The myocardial tissue of the diabetic cardiomyopathy models showed hypertrophy, myocardial fibrosis and collagen deposition. Furthermore, TUNEL staining showed increased apoptosis and decreased expression of STAT4 in the myocardial cells. Moreover, the myocardial tissues of the DCM models showed increased expression of Bax/Bcl-2 and a high percentage of Annexin V positive cells. The H9C2 cells showed decreased expression of STAT4 following high glucose treatment. However, the H9C2 cells overexpressing STAT4 showed decreased expression of Bax/Bcl-2 and reduced percentage of Annexin V positive cells.
Conclusion:
The DCM group had decreased myocardial expression of STAT4. Furthermore, overexpression of STAT4 was shown to reduce high glucose-induced apoptosis.
Insights
Signal transducer and activator of transcription 4 (STAT4) plays a protective role in diabetic cardiomyopathy. Overexpression of STAT4 reduced high glucose-induced apoptosis in H9C2 cells, suggesting its therapeutic potential.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Endocrinology
Background:
- Diabetic cardiomyopathy (DCM) is a complex cardiac dysfunction.
- The role of signal transducer and activator of transcription 4 (STAT4) in DCM remains unclear.
Purpose of the Study:
- To investigate the protective role of STAT4 in diabetic cardiomyopathy.
- To explore the effect of STAT4 on high glucose-induced apoptosis in cardiac cells.
Main Methods:
- Established rat models of diabetic cardiomyopathy using a high-sugar/high-fat diet and streptozotocin.
- Assessed cardiac pathology via HE and Masson's staining.
- Quantified apoptosis using TUNEL and Annexin V assays.
- Investigated STAT4 effects in H9C2 cells with lentiviral overexpression and high glucose treatment, analyzed by CCK-8 and Western blotting.
Main Results:
- DCM rat models exhibited myocardial hypertrophy, fibrosis, and collagen deposition.
- Decreased STAT4 expression and increased apoptosis (TUNEL, Annexin V) were observed in DCM hearts.
- High glucose reduced STAT4 expression in H9C2 cells.
- STAT4 overexpression in H9C2 cells attenuated high glucose-induced apoptosis and modulated Bax/Bcl-2 expression.
Conclusions:
- Diabetic cardiomyopathy is associated with reduced myocardial STAT4 expression.
- STAT4 overexpression demonstrates a protective effect against high glucose-induced apoptosis in cardiac cells.
