CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia-Reperfusion Injury via Inhibiting miRNA-133 Expression

الملخص EN

Objective.

This project is aimed at investigating whether CircANXA2 can promote the apoptosis of myocardial cells by inhibiting miR-133 expression and thereby participate in the development of myocardial ischemia-reperfusion injury.

Materials and Method.

Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression level of CircANXA2 in H9c2 cells after hypoxia/reoxygenation (H/R) treatment.

Evaluation of myocardial injury markers in H9c2 cells was performed using commercial kits, including lactate dehydrogenase (LDH), malonaldehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidation (GSH-PX).

MTT analysis and flow cytometry were used to detect myocardial cell proliferation and apoptosis, respectively.

Western blot was used to detect the protein expression of apoptosis-related genes.

Result.

qRT-PCR results showed that compared with the control, the expression of CircANXA2 was upregulated and the expression level of miR-133 was significantly decreased in H/R-treated H9c2 cells.

CircANXA2 overexpression increased LDH, MDA, SOD, and GSH-PX activity in H/R-treated H9c2 cells.

At the same time, CircANXA2 overexpression inhibited the proliferation of H/R-treated cells, and CircANXA2 was able to induce cardiomyocyte apoptosis.

Western blot results showed that after overexpression of CircANXA2, the proapoptotic genes Bax and cytochrome C was upregulated, while the antiapoptotic gene Bcl-2 was downregulated.

In H9c2 cells, upregulating miR-133 can reverse the inhibition of proliferation induced by CircANXA2 overexpression and increase apoptosis.

Conclusions.

CircANXA2 promotes cardiomyocyte apoptosis in myocardial ischemia-reperfusion injury by inhibiting the expression of miR-133.

CircANXA2 may be a potential target for myocardial ischemia-reperfusion injury.