Background: Myocardial Infarction (MI), a kind of heart deficiency, is the main cause
of death and disability. Autophagy, a metabolic process for the degradation of damaged proteins or
organelles, is important for cardiac functions and regulated by several miRNAs including miRNA-
101. The aim of this research was to investigate the effects of miR-101 in myocardial infarctioninduced
injury and the related mechanisms.
Methods: MI model was induced by ligation of the left coronary artery. The in vitro model was established
by hypoxia-induced H9c2 cells (rat myocardial cells). The overexpression of miR-101
was achieved by transfection. The expression of associated proteins was analyzed by Western blotting.
The level of miR-101 was analyzed by reverse transcription-polymerase chain reaction (RTPCR).
The target genes for miR-101 and the target sites were analyzed by TargetScan.
Results: The results showed that miR-101 was decreased in MI mice (P<0.01). Autophagy and
apoptosis were increased in MI-induced injury (in vivo) and in hypoxia treated myocardial cells (in
vitro) (P<0.01). miR-101 overexpression inhibited the increase of autophagy and apoptosis in mice
and myocardial cells (P<0.01). DDIT4 was a target gene of miR-101 and expressed increasingly in
MI-induced injury mice and hypoxia treated myocardial cells. miR-101 could negatively regulate
the expression of DDIT4.
Conclusion: This research suggested that miR-101 attenuated- MI-induced injury by targeting
DDIT4 to regulate autophagy, which indicated that miR-101 or DDIT4 may be potential therapeutic
targets for heart injury.