MYBL2 protects against H9c2 injury induced by hypoxia via AKT and NF­κB pathways.

ABSTRACT

Cardiovascular diseases have become one of the major public health problems in many countries. The downregulation of MYBL2 was found in H9c2 and native cardiomyocytes cells after hypoxia treatment. The present study aimed to investigate the effects of MYB proto­oncogene like 2 (MYBL2) on H9c2 injury induced by hypoxia. Reverse transcription­quantitative polymerase chain reaction and western blot were performed on H9c2 cells to determine the mRNA and protein levels of MYBL2, respectively. Small interfering RNA (siRNA) was employed to downregulate MYBL2 expression in H9c2 cells to investigate changes in cell proliferation and apoptosis. Cell proliferation was assessed by a Cell Counting kit­8 assay and the percentage of apoptotic cells was determined using an Annexin V­fluorescein isothiocyanate/propidium iodide apoptosis detection kit. The nuclear factor­κB (NF­κB) and AKT signaling pathways in H9c2 cells were investigated by western blot analysis. The results demonstrated that the overexpression of MYBL2 promoted cell proliferation and suppressed apoptosis. Furthermore, overexpression of MYBL2 suppressed the expression of phosphorylated (p)­AKT, p­NF­κB inhibitor α, p­p65 and B­cell CLL/lymphoma 3 (Bcl­3). The results indicated that MYBL2 may improve cell viability and inhibit H9c2 apoptosis via the inhibition of AKT and NF­κB pathways. Therefore, MYBL2 may be a potential therapeutic target for the treatment of myocardial infarction.