This study aims to investigate the molecular mechanism of LncRNA NKILA underlying promoting cardiomyocytes apoptosis and relevant diabetic cardiomyopathy. We utilized high concentration of glucose to induce human cardiomyocytes cell line AC16 to imitate diabetic cardiomyopathy. And then, we performed high-throughput big data analysis, RT-PCR, and western blot assays to evaluate the expression levels of associated mRNA and protein. Cell apoptosis was tested by Annexin V-FITC. The proliferation, migration, and invasion of AC16 cells were examined by CCK8 assay, colony formation assay, EdU assay, wound healing test, and transwell chamber assay. We utilized statistical analysis and luciferase activity assay to analyze the interaction of relevant genes. LncRNA NKILA was highly expressed in AC16 cells induced by high glucose and inhibited AC16 cell proliferation, migration, and invasion by inducing cell apoptosis. Luciferase activity assay demonstrated that LncRNA NKILA binds to miR22-3p. The influence of LncRNA NKILA on AC16 cell proliferation, migration, and invasion could be reversed by miR22-3p. Luciferase activity assay demonstrated that TXNIP was a target of miR-22-3p in AC16 cells, and all the effects of TXNIP on AC16 cell proliferation, migration, and invasion could be abolished by miR22-3p. These results provided comprehensive data about a novel molecular mechanism of LncRNA NKILA promoting cardiomyocytes apoptosis: LncRNA NKILA performed its function in AC16 cells under high glucose-induced condition by targeting mir-22-3p-TXNIP signal axis, which indicated that LncRNA NKILA may play a crucial role in diabetic cardiomyopathy.

中文翻译：

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LncRNA NKILA通过靶向miR22-3p-TXNIP信号轴来抑制高糖诱导条件下心肌细胞的增殖，迁移和侵袭，从而促进心肌细胞凋亡。

这项研究旨在探讨促进心肌细胞凋亡和相关的糖尿病性心肌病的LncRNA NKILA的分子机制。我们利用高浓度的葡萄糖来诱导人心肌细胞AC16细胞来模仿糖尿病性心肌病。然后，我们进行了高通量大数据分析，RT-PCR和western blot分析，以评估相关mRNA和蛋白质的表达水平。通过膜联蛋白V-FITC测试细胞凋亡。通过CCK8分析，集落形成分析，EdU分析，伤口愈合测试和transwell小室分析检查AC16细胞的增殖，迁移和侵袭。我们利用统计分析和荧光素酶活性分析来分析相关基因的相互作用。LncRNA NKILA在高糖诱导的AC16细胞中高表达，并通过诱导细胞凋亡来抑制AC16细胞的增殖，迁移和侵袭。萤光素酶活性测定表明LncRNA NKILA与miR22-3p结合。miR22-3p可以逆转LncRNA NKILA对AC16细胞增殖，迁移和侵袭的影响。萤光素酶活性测定表明，TXNIP是AC16细胞中miR-22-3p的靶标，而miRNA22-3p可以消除TXNIP对AC16细胞增殖，迁移和侵袭的所有作用。这些结果提供了有关LncRNA NKILA促进心肌细胞凋亡的新分子机制的全面数据：LncRNA NKILA通过靶向mir-22-3p-TXNIP信号轴在高葡萄糖诱导的条件下在AC16细胞中发挥其功能，