Effect of TGF-β1 on myocardial cell apoptosis in rats with acute myocardial infarction via MAPK signaling pathway

X.-G. Zhang, Y. Wei, J. Jiang, L. Wang, H.-Y. Liang, C.-B. Lei

Department of Clinical Laboratory, Affiliated Hospital of Weifang Medical College, Weifang, China. fipjwve@163.com

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• Cardiology

OBJECTIVE: Transforming growth factor beta 1 (TGF-β1) can promote myocyte hypertrophy, thus playing an important role in ventricular remodeling after myocardial infarction (MI).

MATERIALS AND METHODS: In this study, the model of MI was established in rats through ligating the left anterior descending coronary artery. Subsequently, the messenger ribonucleic acid (mRNA) and protein expression levels of TGF-β1 in myocardial cells in both model group and sham operation group were determined. The effects of TGF-β1 treatment on myocardial cell apoptosis in MI rats were explored. Moreover, the changes of mitogen-activated protein kinase (MAPK) signaling pathway in rats with acute MI were verified. In addition, the protein expressions of phosphorylated-MAPK kinases 3/6 (p-MKK3/6) and MKK3/6 in myocardial cells of the two groups were analyzed.

RESULTS: The mRNA and protein expression levels of TGF-β1 in myocardial cells of acute MI rats were significantly higher than those in the sham operation group (p<0.01). After treatment with TGF-β1, the expression level of B-cell lymphoma 2 (Bcl-2) associated X protein (Bax) was obviously down-regulated. The Bax/Bcl-2 ratio was notably lower than that in control group (p<0.01). Meanwhile, the proportion of apoptotic cells decreased remarkably (p<0.01). In the model group, no evident change was observed in the protein expression level of MKK3/6, whereas the levels of p-MKK3/6 were prominently up-regulated (p<0.01).

CONCLUSIONS: TGF-β1 can activate MKK3/6 in the MAPK signaling pathway to resist the apoptosis of myocardial cells in acute MI rats.

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