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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Upregulated long noncoding RNA Snhg1 promotes the angiogenesis of brain microvascular endothelial cells after oxygen–glucose deprivation treatment by targeting miR-199a
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Upregulated long noncoding RNA Snhg1 promotes the angiogenesis of brain microvascular endothelial cells after oxygen–glucose deprivation treatment by targeting miR-199a

机译:通过靶向MIR-199A,Uprogulated Long Noncoding RNA SnHG1促进氧血糖剥夺治疗后脑微血管内皮细胞的血管生成

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摘要

Angiogenesis after ischemic stroke has important clinical significance, which stimulates endogenous recovery mechanisms and improves the neurological outcome. Enhancing angiogenesis may facilitate the function recovery from ischemic stroke. Recent studies have shown that aberrant expression of long noncoding RNAs (lncRNAs) is related to angiogenesis after ischemic stroke. Snhg1, a cancer-related lncRNA, has been reported to be upregulated after stroke. However, little is known about its role in stroke. In this study, we performed in vitro experiments to investigate the effects of Snhg1 on cell survival and angiogenesis and molecular mechanism in ischemic stroke. Oxygen–glucose deprivation/reoxygenation (OGD/R) was used to mimic ischemia/reperfusion injury in vitro. Sngh1 was increased in brain microvascular endothelial cells (BMECs) with the prolongation of exposure to OGD, and promoted BMEC survival under OGD/R condition, and angiogenesis after OGD/R treatment. miR-199a was identified and validated to be a direct target of Snhg1, and function effects of Snhg1 on BMEC survival and angiogenesis depended on miR-199a, which is involved in the regulation of hypoxia inducible factor and vascular endothelial cell growth factor expression. These findings contribute to a better understanding of the pathogenesis of ischemic stroke and facilitate the development of proangiogenesis therapy for this disease.
机译:缺血性卒中后的血管生成具有重要的临床意义,其刺激内源性恢复机制并改善神经系统结果。增强血管生成可以促进缺血性卒中的功能恢复。最近的研究表明,长度非编码RNA(LNCRNA)的异常表达与缺血性卒中后的血管生成有关。据报道,SNHG1,癌症相关的LNCRNA,脑卒中后令人兴奋地上调。然而,对其在中风中的作用毫无知之甚少。在本研究中,我们在体外实验中进行了探讨了SNHG1对缺血性卒中细胞存活和血管生成的影响和分子机制。氧葡萄糖剥夺/再氧化(OGD / R)用于模拟体外缺血/再灌注损伤。 SNGH1在脑微血管内皮细胞(BMEC)中升高,随着OGD暴露,并在OGD / R条件下促进BMEC存活,并且在OGD / R处理后血管生成。鉴定MIR-199A并验证是SNHG1的直接靶标,SNHG1对BMEC存活和血管生成的功能效应依赖于MIR-199A,其参与缺氧诱导因子和血管内皮细胞生长因子表达的调节。这些发现有助于更好地理解缺血性卒中的发病机制,促进这种疾病的常规发生治疗的发育。

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