Taxonomic identification, genomic analysis, and optimized chromium(VI) bioreduction by Microbacterium triticisoli sp. nov. M28T.

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.