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Long non-coding RNA KCNQ1OT1/microRNA-204-5p/LGALS3 axis regulates myocardial ischemia/reperfusion injury in mice

机译:长期非编码RNA KcNQ1OT1 / microRNA-204-5P / LGALS3轴调节小鼠心肌缺血/再灌注损伤

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Myocardial ischemia/reperfusion (IR) injury is one of the most prevalent cardiovascular diseases, known for its high mortality and morbidity worldwide. Based on pre-existing evidence, LGALS3 has been found to be closely associated with cardiac diseases. Hence, the objective of our study is to explore the potential function of KCNQ1OT1/microRNA-204-5p (miR-204-5p)/ LGALS3 axis on myocardial IR injury and the underlying mechanism. A myocardial IR injury mouse model was established in vivo and an in vitro cardiomyocyte model was induced by hypoxia/Reoxygenation exposure. Next, gain- and loss-of-function experiments were employed in order to measure the viability and apoptosis of cardiomyocytes and the area of ischemic infarct by CCK-8, TUNEL staining and Evans blue/TTC double staining. LGALS3 was found to be highly expressed in myocardial IR injury. The downregulation of LGALS3 resulted in the alleviation of myocardial IR injury in mouse models. In addition, KCNQ1OT1 could promote the LGALS3 expression by binding to miR-204-5p, which led to aggravated myocardial IR injury. In conclusion, KCNQ1OT1 binds to miR-204-5p to exacerbate myocardial IR injury in mice through the up-regulation of LGALS3, providing a novel insight for myocardial IR injury treatment.
机译:心肌缺血/再灌注(IR)损伤是最普遍的心血管疾病之一,以其在全球性的高死亡率和发病率而闻名。基于预先存在的证据,已发现LGALS3与心脏病密切相关。因此,我们的研究目的是探讨KCNQ1OT1 / microRNA-204-5P(MIR-204-5P)/ LGALS3轴在心肌红外损伤和潜在机制的潜在功能。在体内建立了一种心肌红外损伤小鼠模型,缺氧/雷诺化暴露诱导了体外心肌细胞模型。接下来,采用增益和功能丧失实验,以测量CCK-8,TUNEL染色和evans蓝/ TTC双染色的心肌细胞和缺血性梗塞面积的活力和凋亡。发现LGALS3在心肌红外损伤中高度表达。 LGALS3的下调导致小鼠模型中心肌红外损伤的减轻。此外,KCNQ1OT1可以通过结合miR-204-5p来促进LGALS3表达,这导致了加重心肌红外损伤。总之,KCNQ1OT1通过LGALS3的上调结合MIR-204-5P,在小鼠中加剧小鼠心肌红外损伤,为心肌红​​外损伤治疗提供了一种新颖的洞察力。

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