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.
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.
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DOI：
10.4049/jimmunol.0902369
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发表时间：
2010-01-01
期刊：
影响因子：
--
通讯作者：
Pober JS
中科院分区：
文献类型：
--
作者：
Suárez Y;Wang C;Manes TD;Pober JS
微小RNA（miRNAs）与mRNA的3 'UTR中的靶序列配对以转录后抑制基因表达。在这里，我们报告说，TNF介导的诱导内皮细胞粘附分子可以调节由TNF诱导的miRNA。具体而言，E-选择素和ICAM-1分别是TNF诱导的miRNAs miR-31和miR-17- 3 p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EC的粘附。相反，用这些miRNAs的模拟物转染减少了中性粒细胞对EC的粘附。这些数据表明，miRNA提供炎症的负反馈控制。
MicroRNAs (miRNAs) pair with target sequences in the 3’UTR of mRNAs to post-transcriptionally repress gene expression. Here 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 ECs. Conversely, transfections with mimics of these miRNAs decreased neutrophil adhesion to ECs. These data suggest that miRNAs provide negative feedback control of inflammation.
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