Up-regulation of miR-203 expression induces endothelial inflammatory response: Potential role in preeclampsia

被引:28
|
作者
Wang, Yuping [1 ]
Dong, Qin [1 ]
Gu, Yang [1 ]
Groome, Lynn J. [1 ]
机构
[1] Louisiana State Univ, Dept Obstet & Gynecol, Hlth Sci Ctr, Shreveport, LA 71105 USA
关键词
adhesion molecule; endothelial cells; inflammatory response; miR-203; preeclampsia; SOCS-3; CYTOKINE SIGNALING SOCS; NEGATIVE REGULATORS; ADHESION MOLECULE; MICRORNA-203; CELLS; ACTIVATION; PROTEINS; PLASMA; SUPPRESSORS; PLACENTAS;
D O I
10.1111/aji.12589
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
ProblemTo determine whether miR-203 mediates endothelial inflammatory response in preeclampsia. Method of studyMaternal vessel miR-203 expression was assessed by in situ hybridization. Suppressor of cytokine signaling-3 (SOCS-3) and ICAM expression was determined by immunostaining. Subcutaneous fat tissue sections from normal and preeclamptic pregnant women were used. miR-203-induced inflammatory response was evaluated by the measurements of IL-6, IL-8, ICAM, and VCAM expression and production and neutrophil adhesion in the endothelial cells (EC) transfected with miR-203 precursor, pre-miR-203. SOCS3 expression was also determined. ResultsUp-regulation of miR-203 and ICAM expression and down-regulation of SOCS-3 expression were demonstrated in maternal vessel endothelium in preeclampsia. Overexpression of miR-203 resulted in down-regulation of SOCS-3 expression and increases in the production of IL-6, IL-8, ICAM, and VCAM and neutrophil adhesion in ECs. ConclusionAs miR-203 is an inflammatory microRNA, increased miR-203 production/expression in ECs could diminish an anti-inflammatory activity and increase the endothelial inflammatory response in preeclampsia.
引用
收藏
页码:482 / 490
页数:9
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