lncRNA UCA1抑制miR-503减轻缺氧诱导的心肌细胞损伤机制研究

孝俊; 柴晓莉; 李念; 李琼

doi:10.13898/j.cnki.issn.1000-2200.2022.02.005

lncRNA UCA1抑制miR-503减轻缺氧诱导的心肌细胞损伤机制研究

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

摘要

摘要:
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UCA1过表达载体、miR-503抑制物分别转染AC16，检测上调UCA1或下调miR-503对缺氧条件下AC16细胞增殖和凋亡的影响。双荧光素酶报告基因实验和RT-qPCR确定UCA1对miR-503的靶向作用。
结果缺氧处理后AC16细胞存活率、S期细胞比例降低，凋亡率、G₀~G₁期细胞比例升高，差异均有统计学意义（P < 0.05）。上调UCA1或下调miR-503表达后，缺氧处理的AC16细胞存活率、S期细胞比例升高，凋亡率、G₀~G₁期细胞比例降低，差异均有统计学意义（P < 0.05）。miR-503是UCA1的靶基因，UCA1负性调控miR-503表达。
结论lncRNA UCA1能够显著提高缺氧条件下心肌细胞存活率，抑制缺氧诱导的心肌细胞凋亡，其机制可能与靶向下调miR-503表达有关。

Abstract:
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.

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