前沿：TNF 诱导的 microRNAs 调节人内皮细胞上 TNF 诱导的 E-选择素和细胞间黏附分子-1 的表达：炎症的反馈控制。
Cutting edge: TNF-induced microRNAs regulate TNF-induced expression of E-selectin and intercellular adhesion molecule-1 on human endothelial cells: feedback control of inflammation.
机构信息
Department of Immunobiology and Interdepartmental Program in Vascular Biology and Therapeutics, Yale University School of Medicine, New Haven, CT 06520-8089, USA.
出版信息
J Immunol. 2010 Jan 1;184(1):21-5. doi: 10.4049/jimmunol.0902369. Epub 2009 Nov 30.
Abstract
MicroRNAs (miRNAs) pair with target sequences in the 3' untranslated region of mRNAs to posttranscriptionally repress gene expression. In this study, we report that TNF-mediated induction of endothelial adhesion molecules can be regulated by miRNAs that are induced by TNF. Specifically, E-selectin and ICAM-1 are targets of TNF-induced miRNAs miR-31 and miR-17-3p, respectively. Specific antagonism of these TNF-induced miRNAs increased neutrophil adhesion to cultured endothelial cells. Conversely, transfections with mimics of these miRNAs decreased neutrophil adhesion to endothelial cells. These data suggest that miRNAs provide negative feedback control of inflammation.
摘要
MicroRNAs (miRNAs) 与 mRNA 的 3'非翻译区的靶序列配对，从而在后转录水平抑制基因表达。在这项研究中，我们报告说，TNF 介导的内皮细胞黏附分子的诱导可以通过 TNF 诱导的 miRNA 来调节。具体而言，E-选择素和 ICAM-1 分别是 TNF 诱导的 miRNA miR-31 和 miR-17-3p 的靶标。这些 TNF 诱导的 miRNA 的特异性拮抗作用增加了中性粒细胞对培养的内皮细胞的黏附。相反，用这些 miRNA 的模拟物转染会降低中性粒细胞对内皮细胞的黏附。这些数据表明，miRNAs 提供了炎症的负反馈控制。
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