MicroRNAs have been shown to play critical regulatory roles in various ischemia/reperfusion (I/R) injury.
However, its role in myocardial I/R injury remains largely unknown. The aim of this study was to investigate the role
of microRNA-34a (miR-34a) in the development of myocardial I/R injury. Rat myocardial I/R model was established,
followed by PCR array analyses to investigate the expressional alterations of miRNAs in the hearts of rats. H9c2
cardiomyocytes were subjected to hypoxia/reoxygenation (H/R), and lactate dehydrogenase (LDH) release, cell vi
-
ability and rat cardiomyocyte apoptosis were measured as well as miR-34a expression. Knockdown experiments
were performe... More
MicroRNAs have been shown to play critical regulatory roles in various ischemia/reperfusion (I/R) injury.
However, its role in myocardial I/R injury remains largely unknown. The aim of this study was to investigate the role
of microRNA-34a (miR-34a) in the development of myocardial I/R injury. Rat myocardial I/R model was established,
followed by PCR array analyses to investigate the expressional alterations of miRNAs in the hearts of rats. H9c2
cardiomyocytes were subjected to hypoxia/reoxygenation (H/R), and lactate dehydrogenase (LDH) release, cell vi
-
ability and rat cardiomyocyte apoptosis were measured as well as miR-34a expression. Knockdown experiments
were performed to determine the effects of manipulating miR-34a on apoptotic responses. Our results revealed that
miR-34a was significantly up-regulated in I/R group compared with sham group. Inhibition of miR-34a promoted cell
proliferation, reduced LDH release and apoptosis which were accompanied by a significant decrease in caspase-3
activity. Furthermore, Bcl-2, a well know anti-apoptotic gene was identified to be a functional target of miR-34a.
Taken together, knockdown of miR-34a mediates H/R-induced apoptosis in cardiomyocytes by targeting Bcl-2 and
represents a potential target for prevention of myocardial I/R injury
