LncRNA-ROR alleviates hypoxia-triggered damages by downregulating miR-145 in rat cardiomyocytes H9c2 cells.

Chronic hypoxic heart disease (CHD) is a common clinical type of congenital heart disease. Long noncoding RNA regulator of reprogramming (lncRNA-ROR) exerts an important regulating effect in cardiovascular diseases. In our study, we explored the effect of lncRNA-ROR and the possible mechanisms against hypoxia-caused apoptosis in H9c2 cells. H9c2 cells were exposed to hypoxia (1% O2 ) to construct the in vitro model of CHD. The level of lncRNA-ROR and microRNA (miRNA/miR)-145 was detected. To upregulate the level of lncRNA-ROR and miR-145, transfection was carried out. Western blot assay was performed to quantified protein expression. The interaction of lncRNA-ROR with miR-145 was verified by RIP and Dual-luciferase reporter assays. The expression of p53 and Bax was largely elevated and Bcl-2 was suppressed by hypoxia induction. We found that lncRNA-ROR was elevated by hypoxia. LncRNA-ROR overexpression was able to relieve the damages of H9c2 cells induced by hypoxia through rescuing viability, suppressing apoptosis, and blocking Cytochrome c release. miR-145 was suppressed by overexpressed lncRNA-ROR and the combination of miR-145 mimic was able to abolish the protective effect of lncRNA-ROR. Moreover, we found that lncRNA-ROR activated Ras/Raf/MEK/ERK and PI3K/AKT transduction cascades by suppressing miR-145. Besides, lncRNA-ROR directly targeted miR-145 and negatively modulated the level of miR-145. Our present study revealed that lncRNA-ROR protected H9c2 cells against hypoxia-caused damages by regulation of miR-145 through activating Ras/Raf/MEK/ERK and PI3K/AKT.