Myocardial infarction (MI) is highly lethal as it leads to cardiac decompensation and ultimately to heart failure. Long noncoding RNAs (LncRNAs) play crucial regulatory roles in cardiovascular disease. In the present research, the expression pattern of LncRNAs and mRNAs in the Sprague‐Dawley (SD) rat model of MI was described by microarray technology. RT‐qPCR was adopted to evaluate the expression of candidate LncRNAs. H9c2 cells were used to construct ischemic and hypoxic models to simulate MI in vitro. The expression of autophagy‐related proteins was determined via Western blot. Flow cytometry assay was conducted for the detection of apoptotic cells. CCK‐8 assay was applied to examine the cell viability. Fluorescence microscopy of GFP‐LC3 puncta was used to analyze autophagosome formation. Compared with the control group, 75 LncRNAs and 331 mRNAs were differentially expressed in the MI group. Among these, LOC100911723 was found to be significantly upregulated in the MI group. Knockdown of LOC100911723 significantly promoted the cell viability of H9c2 cells and attenuated ischemic hypoxia–induced apoptosis. In addition, knockdown of LOC100911723 suppressed cell autophagy of H9c2 cells. In conclusion, knockdown of LOC100911723 attenuated apoptosis and autophagy in ischemic–hypoxic cardiomyocytes, and LOC100911723 may be a key target for effective mitigation of MI injury.
Liu et al. (Thu,) studied this question.