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.

中文翻译：

---

长非编码 RNA LINC00261 的下调通过 miR-522-3p/含有三核苷酸重复的基因 6a (TNRC6A) 轴减轻心肌梗塞


背景。心肌梗死（MI）是冠状动脉急性持续缺血性缺氧引起的心脏组织坏死。本研究旨在探讨长非编码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检测正常细胞和MI细胞中LINC00261、miR-522-3p和TNRC6A的表达水平。 Western blotting分析检测TNRC6A蛋白的表达。检测敲除LINC00261或TNRC6A后MI后心肌细胞的活力和凋亡。使用双荧光素酶报告基因测定评估心肌细胞中 miR-522-3p、LINC00261 和 TNRC6A 之间的关系。采用正常细胞缺氧预处理构建模拟心肌梗死环境，研究LINC00261对心肌细胞凋亡的影响。结果。在伴有 MI 的冠心病组织中，LINC00261 和 TNRC6A 上调，而 miR-522-3p 下调。敲除LINC00261可以增加心肌细胞的活力并抑制细胞凋亡。 LINC00261 靶向心肌细胞中的 miR-522-3p。此外，miR-522-3p 还靶向心肌细胞中的 TNRC6A。 TNRC6A 调节 MI 后心肌细胞的细胞活力和凋亡，并且 TNRC6A 诱导的 MI 可以通过 miR-522-3p 的过表达来逆转。结论。 LINC00261 通过直接靶向 miR-522-3p 下调 MI 后心肌细胞中的 miR-522-3p。 TNRC6A 是 miR-522-3p 的直接靶标。我们的结果表明 LINC00261 可能作为 MI 治疗的治疗靶点。