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Long non-coding RNA LOC285194 regulates vascular smooth muscle cell apoptosis in atherosclerosis

机译:长期非编码RNA LOC285194调节动脉粥样硬化的血管平滑肌细胞凋亡

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摘要

Long non-coding RNAs (lncRNAs) recently have been implicated in many biological processes and diseases. Atherosclerosis is a major risk factor for cardiovascular disease. However, the functional role of lncRNAs in atherosclerosis is largely unknown. Here we identified LOC285194 as a key regulator of cell proliferation and apoptosis during atherosclerosis. The expression of LOC285194 was dramatically down-regulated in a aortic atherosclerotic plaques of well-defined model of apolipoprotein-E knockout (ApoE−/-) mice. Moreover, we found that targeting LOC285194 results in neointimal hyperplasia in vivo in carotid artery injury model. We also showed that targeting LOC285194 promotes cell proliferation and inhibits apoptosis in vascular smooth muscle cells (VSMCs) in vitro, and vice versa. In addition, targeting LOC285194 promotes cell invasion and migration in vitro. Our studies identify LOC285194 as a novel regulator of cell proliferation and apoptosis and suggest that this lncRNA could serve as a therapeutic target to treat atherosclerosis and related cardiovascular disorders.
机译:最近长期的非编码RNA(LNCRNA)涉及许多生物过程和疾病。动脉粥样硬化是心血管疾病的主要危险因素。然而,LNCRNA在动脉粥样硬化中的功能作用在很大程度上是未知的。在这里,我们将LOC285194鉴定为动脉粥样硬化期间细胞增殖和细胞凋亡的关键调节因子。 LOC285194的表达在载脂蛋白-E敲除(ApoE - / - )小鼠的明确定义模型的主动脉动脉粥样硬化斑块中显着下调。此外,我们发现靶向LOC285194导致颈动脉损伤模型体内内膜增生。我们还表明,靶向LOC285194促进细胞增殖并抑制体外血管平滑肌细胞(VSMC)的凋亡,反之亦然。此外,靶向LOC285194促进细胞侵袭和体外迁移。我们的研究将LOC285194鉴定为细胞增殖和细胞凋亡的新型调节因子,并表明该LNCRNA可以作为治疗动脉粥样硬化和相关心血管病症的治疗靶标。

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