Background: This study aimed to investigate the effect of long non-coding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1) on cell proliferation and apoptosis in myocardial ischemia/reperfusion (I/R) injury cells, and explore its target miRNAs.
Methods: H9c2 cells were cultured in oxygen and glucose deprivation followed by reperfusion (OGD/R) condition to construct a myocardial I/R injury model. Blank shRNA and lnc-NEAT1 shRNA were transferred into normal H9c2 cells and I/R injury H9c2 cells as Normal&sh-NC, OGD/R&sh-NC and OGD/R&sh-NEAT1 groups. Rescue experiment was performed by transfection of NC inhibitor plasmids, miR-193a inhibitor plasmids and NEAT1 shRNA into I/R injury cardiocytes. RNA expression, cell proliferation and cell apoptosis rate were detected by qPCR, CCK-8 and AV/PI respectively.
Results: After OGD/R induction, H9c2 cell apoptosis was greatly increased while cell proliferation was decreased, which indicated successful establishment of myocardial I/R injury model, and lnc-NEAT1 expression was elevated as well. Cell proliferation rate was increased in OGD/R&sh-NEAT1 group at 48 h and 72 h compared to OGD/R&sh-NC group, while cell apoptosis was reduced in OGC/R&sh-NEAT1 group compared to OGD/R&sh-NC group. Target miRNAs detection indicated the negative regulation of lnc-NEAT1 on miR-193a but not miR-182 or miR-141. In rescue experiment, downregulation of lnc-NEAT1 promoted cell proliferation and inhibited cell apoptosis through targeting miR-193a in I/R injury H9c2 cells.
Conclusion: Lnc-NEAT1 is overexpressed in myocardial I/R injury cells compared to normal myocardial cells, and downregulation of lnc-NEAT1 enhances cell proliferation while inhibits cell apoptosis through targeting miR-193a in I/R injury H9c2 cells.
Keywords: Cell apoptosis; Cell proliferation; Long non-coding RNA nuclear enriched abundant transcript 1; Myocardial ischemia/reperfusion injury; miR-193a.