Hyperglycemia is an important initiator of
cardiovascular disease, contributing to the development of
cardiomyocyte death and
diabetic complications. The purpose of the present study was to investigate whether high
glucose state could induce
apoptosis of
rat cardiomyocyte cell line H9c2 through
microRNA-mediated Bcl-2 signaling pathway. The expression of miR-34a and Bcl-2
mRNA was detected by using
real-time PCR.
Western blotting was used to examine the changes in
apoptosis-associated
protein Bcl-2.
Apoptosis of H9c2
cells was tested by using
flow cytometry. The results showed that the expression of miR-34a was significantly elevated and that of Bcl-2 was strongly reduced, and
apoptosis of
cardiomyocytes was apparently increased in the high-
glucose-treated H9c2
cells as compared with normal-
glucose-treated controls. In addition, we identified
Bcl-2 gene was the target of miR-34a. miR-34a mimics reduced the expression of Bcl-2 and increased
glucose-induced
apoptosis, but miR-34a inhibitor acted as the opposite mediator. Our data demonstrate that miR-34a contributes to high
glucose-induced decreases in Bcl-2 expression and subsequent
cardiomyocyte apoptosis.