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

Up-regulation of miR-203 expression induces endothelial inflammatory response: Potential role in preeclampsia.
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miR-203 表达上调诱导内皮炎症反应:在先兆子痫中的潜在作用。

DOI:
10.1111/aji.12589
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发表时间:
2016-12
期刊:
American journal of reproductive immunology (New York, N.Y. : 1989)
影响因子:
--
通讯作者:
Groome LJ
Groome LJ
中科院分区:
其他
文献类型:
--
作者:
Wang Y;Dong Q;Gu Y;Groome LJ

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确定miR-203是否介导子痫前期的内皮炎症反应。原位杂交检测母体血管miR-203的表达。免疫染色法检测细胞因子信号传导抑制因子-3 (SOCS-3)和ICAM的表达。使用正常和子痫前期孕妇的皮下脂肪组织切片。通过测量转染MiR-203前体pre-miR-203的内皮细胞(EC)中IL-6、IL-8、ICAM和VCAM的表达和产生,以及中性粒细胞粘附,评估MiR-203诱导的炎症反应。测定SOCS3的表达。子痫前期母体血管内皮中miR-203和ICAM表达上调,SOCS-3表达下调。过表达miR-203导致细胞中SOCS-3表达下调,IL-6、IL-8、ICAM和VCAM的产生增加,中性粒细胞粘附增加。由于miR-203是一种炎症性microRNA,在ECs中miR-203的产生/表达增加可能会降低子痫前期内皮细胞的抗炎活性,增加内皮细胞的炎症反应。
To determine if miR-203 mediates endothelial inflammatory response in preeclampsia. 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 measurements of IL-6, IL-8, ICAM, and VCAM expression and production, and neutrophil adhesion in endothelial cells (EC) transfected with miR-203 precursor, pre-miR-203. SOCS3 expression was also determined. Up-regulation of miR-203 and ICAM expression and down-regulation of SOCS-3 expression was demonstrated in maternal vessel endothelium in preeclampsia. Over-expression of miR-203 resulted in down-regulation of SOCS-3 expression and increases in production of IL-6, IL-8, ICAM and VCAM, and neutrophil adhesion in ECs. As miR-203 is an inflammatory microRNA, increased miR-203 production/ expression in ECs could diminish anti-inflammatory activity and increase endothelial inflammatory response in preeclampsia.
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