lncRNA UCA1抑制miR-503减轻缺氧诱导的心肌细胞损伤机制研究

目的:探讨长链非编码RNA(lncRNA)尿路上皮癌相关1(UCA1)靶向miR-503对缺氧条件下心肌细胞增殖、凋亡的影响.方法:构建体外心肌细胞AC16缺氧模型.实时荧光定量PCR(RT-qPCR)检测UCA1和miR-503表达.细胞计数试剂盒(CCK-8)检测细胞活力;流式细胞术检测细胞凋亡和周期分布.将UCA...

lncRNA UCA1 alleviates hypoxia-induced cardiomyocyte injury by targeting miR-503

ObjectiveTo investigate the effect of long-chain non-coding RNA(lncRNA) urothelial carcinoma is associated 1(UCA1) targeting miR-503 on proliferation and apoptosis of cardiomyocyte with hypoxia treatment.MethodsThe cardiomyocyte AC16 hypoxia model was established in vitro.The expression of UCA1 and miR-503 were detected by real-time quantitative PCR (RT-qPCR).The cell viability was measured by CCK-8.Apoptosis and cycle distribution were detected by flow cytometry.The UCA1 overexpression vector and miR-503 inhibitor were transfected into AC16 cells, respectively.And the effects of up-regulating UCA1 or down-regulating miR-503 on the proliferation and apoptosis of AC16 cells treated with hypoxic were detected.Dual luciferase reporter gene assay and RT-qPCR confirmed the targeting effect of UCA1 on miR-503.ResultsAfter treated with hypoxia, the survival rate of AC16 cells and the proportion of S-phase cells were significantly decreased, and the apoptosis rate and the proportion of G₀-G₁ phase cells were significantly increased (P < 0.05).After up-regulating UCA1 expression or down-regulating miR-503 expression, the survival rate and the proportion of S-phase in AC16 cells treated with hypoxia were significantly increased, while the apoptosis rate and the proportion of G₀-G₁ phase cells were significantly decreased (P < 0.05).miR-503 was the target gene of UCA1, and UCA1 negatively regulated the expression of miR-503.ConclusionslncRNA UCA1 can significantly improve the survival rate and inhibit the apoptosis in hypoxia-induced cardiomyocyte, which may be attributed to the targeted down-regulation of miR-503 expression.