细胞生物学
细胞粘附分子
PI3K/AKT/mTOR通路
单核细胞
内皮干细胞
细胞粘附
脐静脉
蛋白激酶B
信号转导
内皮
粘附
医学
免疫学
癌症研究
生物
化学
内科学
生物化学
体外
有机化学
作者
Xianlong Li,Qian Zhang,Rui Zhang,Nan Cheng,Na Guo,Yiqian Liu,Jun Cai,Ding Yuan
标识
DOI:10.1016/j.thromres.2019.05.009
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.We obtained human umbilical vein endothelial cells (HUVECs) from patients with or without PIH. Different methods, such as inhibitors: oleamide and Gap26, or specific siRNA were used to alter Cx43 channels function or protein expression in normal or PIH-HUVECs. U937-HUVECs adhesion, adhesion molecules expression, such as VCAM-1 and ICAM-1, and the activity of PI3K/AKT/NF-κB signaling pathway were determined.Monocyte-endothelial adhesion on PIH-HUVECs was much more obvious than that on normal HUVECs. Inhibition of Cx43 protein expression could attenuate cell adhesion significantly, however, function of Cx43 channels had no effects on it. Alternation of Cx43 protein expression on PIH-HUVECs mediated VCAM-1 and ICAM-1 expression via regulating the activity of PI3K/AKT/NF-κB signaling pathway.We firstly reported Cx43 protein expression on PIH-HUVECs was much higher than that on normal HUVECs. Elevation of Cx43 protein expression within the vasculature resulted in PI3K/AKT/NF-κB signaling pathway activation and VCAM-1 and ICAM-1 over-expression, which ultimately lead to monocyte-endothelial adhesion increase.
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