Dilated cardiomyopathy (DCM) is the leading cause of morbidity and mortality in diabetic patients. Long noncoding RNA plasmacytoma variant translocation 1 (PVT1) has been shown to be related to the pathogenesis of DCM. However, the mechanism by which PVT1 regulates DCM pathogenesis is unclear. High glucose level was employed to construct a DCM cell model in vitro. Cell viability was determined via cell counting kit‐8 assay. The level of lactate dehydrogenase (LDH) was measured with the corresponding kit. Expression levels of PVT1, miR‐23a‐3p, and caspase‐10 (CASP10) messenger RNA were evaluated with a quantitative real‐time polymerase chain reaction. Cell apoptosis was assessed by flow cytometry assay. Protein levels of B‐cell lymphoma 2‐associated X (Bax), cleaved‐caspase‐3 (cleaved‐casp‐3), and CASP10 were examined via western blot analysis. The relationship between PVT1 or CASP10 and miR‐23a‐3p was verified with dual‐luciferase reporter assay. We observed that PVT1 and CASP10 were upregulated while miR‐23a‐3p was downregulated in high glucose‐induced cardiomyocytes. High glucose levels repressed cardiomyocyte activity and induced cardiomyocyte apoptosis, but this influence was antagonized by PVT1 knockdown or miR‐23a‐3p overexpression. Furthermore, PVT1 acted as a sponge for miR‐23a‐3p, and miR‐23a‐3p inhibition counterbalanced the influence of PVT1 silencing on viability and apoptosis of cardiomyocytes under high glucose level treatment. PVT1 could increase CASP10 expression via sponging miR‐23a‐3p. In conclusion, PVT1 acted as a deleterious lncRNA in DCM. PVT1 facilitated cardiomyocyte death by regulating the miR‐23a‐3p/CASP10, which offered a new mechanism to comprehend the pathogenesis of DCM.

中文翻译：

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长链非编码 RNA PVT1 通过 miR-23a-3p/CASP10 轴促进高糖诱导的心肌细胞死亡

扩张型心肌病 (DCM) 是糖尿病患者发病率和死亡率的主要原因。长链非编码 RNA 浆细胞瘤变异易位 1 (PVT1) 已被证明与 DCM 的发病机制有关。然而，PVT1 调节 DCM 发病机制的机制尚不清楚。采用高葡萄糖水平在体外构建DCM细胞模型。通过细胞计数试剂盒-8 测定确定细胞活力。用相应的试剂盒测量乳酸脱氢酶（LDH）的水平。通过定量实时聚合酶链反应评估 PVT1、miR-23a-3p 和 caspase-10 (CASP10) 信使 RNA 的表达水平。通过流式细胞术测定评估细胞凋亡。通过蛋白质印迹分析检查 B 细胞淋巴瘤 2 相关 X (Bax)、cleaved-caspase-3 (cleaved-casp-3) 和 CASP10 的蛋白质水平。PVT1 或 CASP10 与 miR-23a-3p 之间的关系通过双荧光素酶报告基因检测验证。我们观察到在高糖诱导的心肌细胞中 PVT1 和 CASP10 上调而 miR-23a-3p 下调。高葡萄糖水平抑制心肌细胞活性并诱导心肌细胞凋亡，但这种影响被 PVT1 敲低或 miR-23a-3p 过表达所拮抗。此外，PVT1 充当 miR-23a-3p 的海绵，抑制 miR-23a-3p 抵消了 PVT1 沉默对高糖水平处理下心肌细胞活力和凋亡的影响。PVT1 可以通过海绵 miR-23a-3p 增加 CASP10 的表达。总之，PVT1 在 DCM 中充当了有害的 lncRNA。PVT1 通过调节 miR-23a-3p/CASP10 促进心肌细胞死亡，