子痫前期
炎症反应
细胞生物学
小RNA
炎症
内皮功能障碍
免疫学
癌症研究
医学
生物
内科学
怀孕
遗传学
基因
作者
Yuping Wang,Qian Dong,Yang Gu,Lynn J. Groome
摘要
Problem To determine whether miR‐203 mediates endothelial inflammatory response in preeclampsia. Method of study Maternal 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. SOCS 3 expression was also determined. Results Up‐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 EC s. Conclusion As miR‐203 is an inflammatory micro RNA , increased miR‐203 production/expression in EC s could diminish an anti‐inflammatory activity and increase the endothelial inflammatory response in preeclampsia.
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