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首页> 外文期刊>BMC Molecular Biology >MicroRNA-19a regulates lipopolysaccharide-induced endothelial cell apoptosis through modulation of apoptosis signal-regulating kinase 1 expression
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MicroRNA-19a regulates lipopolysaccharide-induced endothelial cell apoptosis through modulation of apoptosis signal-regulating kinase 1 expression

机译:MicroRNA-19a通过调节细胞凋亡信号调节激酶1表达来调节脂多糖诱导的内皮细胞凋亡

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MicroRNAs, small non-encoding RNAs that post-transcriptionally modulate expression of their target genes, have been implicated as critical regulatory molecules in endothelial cells. In the present study, we found that overexpression of miR-19a protects endothelial cells from lipopolysaccharide (LPS)-induced apoptosis through the apoptosis signal-regulating kinase 1 (ASK1)/p38 pathway. Quantitative real-time PCR demonstrated that the expression of miR-19a in endothelial cell was markedly down-regulated by LPS stimulation. Furthermore, LPS-induced apoptosis was significantly inhibited by over-expression of miR-19a. Finally, both a luciferase reporter assay and western blot analysis showed that ASK1 is a direct target of miR-19a. MiR-19a regulates ASK1 expression by targeting specific binding sites in the 3’ untranslated region of ASK1 mRNA. Overexpression of miR-19a is an effective method to protect against LPS-induced apoptosis of endothelial cells.
机译:MicroRNA是转录后调节其靶基因表达的小型非编码RNA,已被认为是内皮细胞中的关键调控分子。在本研究中,我们发现miR-19a的过表达通过凋亡信号调节激酶1(ASK1)/ p38途径保护内皮细胞免受脂多糖(LPS)诱导的凋亡。实时定量PCR证实,LPS刺激可显着下调内皮细胞中miR-19a的表达。此外,miR-19a的过表达显着抑制了LPS诱导的细胞凋亡。最后,荧光素酶报告基因分析和蛋白质印迹分析均显示ASK1是miR-19a的直接靶标。 MiR-19a通过靶向ASK1 mRNA 3'非翻译区的特异性结合位点来调节ASK1表达。 miR-19a的过表达是防止LPS诱导的内皮细胞凋亡的有效方法。

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