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Down-regulation of Cx43 expression on PIH-HUVEC cells attenuates monocyte-endothelial adhesion.

Thromb. Res.. 2019-07; 
LiXianlong,ZhangQian,ZhangRui,ChengNan,GuoNa,LiuYiqian,CaiJun,YuanDong
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Peptide Synthesis HUVECs were pretreated with inhibitors of Cx43, oleamide (50 μM, 1 h or 24 h, Sigma-Aldrich), Gap26 (VCYDKSFPISHVR, 300 μM, 1 h, GenScript, Nanjing, China) or Gap26 scrambled peptide sequence (Gap26-SPS, VCYDQAFPISHIR, 300 μM, 1 h, GenScript). Get A Quote

摘要

Pregnancy-induced hypertension (PIH) is the most common serious complication of pregnancy, resulting in significant maternal and fetal morbidity and mortality. Vasospasm is the main pathogenesis of PIH, which leads to the hemodynamic changes and the injury of vascular endothelial cells. However, the underlying mechanism is still unclear. Monocyte-endothelial adhesion is always considered to be one of the most important indicators of vascular endothelial cell injury. Connexin43 (Cx43) plays an important part in monocyte-endothelial adhesion. Thus, we explored effects of Cx43 on cell adhesion in PIH-induced vascular endothelial cells injury.

关键词

Connexin43,PI3K/AKT/NF-κB signaling pathway,Pregnancy-induced hypertension,intercellular adhesion molecule 1,monocyte–endothelial adhesion,vascular cell adhesion molecu