长链非编码 RNA LINC00261 的下调通过 miR-522-3p/三核苷酸重复序列包含基因 6a（TNRC6A）轴减轻心肌梗死。
Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis.
机构信息
Department of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, China.
Department of Clinical Laboratory, The Third Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510240, China.
出版信息
Cardiovasc Ther. 2021 Jun 18;2021:6628194. doi: 10.1155/2021/6628194. eCollection 2021.
BACKGROUND
Myocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells.
METHODS
qRT-PCR was performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells. Western blotting analysis was performed to detect the expression of TNRC6A protein. Viability and apoptosis of myocardial cells after MI with the knockout of LINC00261 or TNRC6A were detected. The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay. Hypoxic preconditioning in normal cells was used to construct a simulated MI environment to investigate the effect of LINC00261 on apoptosis of cardiac cells.
RESULTS
LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI. Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p.
CONCLUSIONS
LINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p. Our results indicated that LINC00261 might serve as a therapeutic target for the treatment of MI.
背景
心肌梗死（MI）是由于冠状动脉急性和持续缺血缺氧导致的心肌组织坏死。本研究旨在探讨长链非编码 RNA（lncRNA）LINC00261 在 MI 中的表达及其对心肌细胞的影响。
方法
采用 qRT-PCR 检测正常和 MI 细胞中 LINC00261、miR-522-3p 和 TNRC6A 的表达水平。采用 Western blot 分析检测 TNRC6A 蛋白的表达。检测敲除 LINC00261 或 TNRC6A 后 MI 心肌细胞的活力和凋亡。采用双荧光素酶报告基因检测评估心肌细胞中 miR-522-3p、LINC00261 和 TNRC6A 之间的关系。用正常细胞缺氧预处理构建模拟 MI 环境，研究 LINC00261 对心脏细胞凋亡的影响。
结果
冠心病合并 MI 组织中 LINC00261 和 TNRC6A 上调，miR-522-3p 下调。敲除 LINC00261 可增加心肌细胞活力，抑制细胞凋亡。LINC00261 在心肌细胞中靶向 miR-522-3p。此外，miR-522-3p 在心肌细胞中靶向 TNRC6A。TNRC6A 调节 MI 后心肌细胞的活力和凋亡，过表达 miR-522-3p 可逆转 TNRC6A 诱导的 MI。
结论
MI 后 LINC00261 通过直接靶向 miR-522-3p 下调心肌细胞中的 miR-522-3p。TNRC6A 是 miR-522-3p 的直接靶标。我们的研究结果表明，LINC00261 可能成为治疗 MI 的治疗靶点。
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