【摘 要】
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Intercellular communication through gap junctions plays an essential role in maintaining the functional integrity of vascular endothelium.Despite emerging evidence suggests that advanced glycation end
【出 处】
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第五届钱江国际心血管病会议暨2011浙江省心血管病年会
论文部分内容阅读
Intercellular communication through gap junctions plays an essential role in maintaining the functional integrity of vascular endothelium.Despite emerging evidence suggests that advanced glycation end products (AGEs) may impair endothelial function.However, its effect on connexin43(Cx43) gap junction in endothelial cells remains unexplored.Here we investigated the effectof AGEbovine serum albumin (AGE-BSA) on Cx43 gap junction in endothelial cells.The levels of Cx43 protein in human umbilical vein endothelial cells (HUVECs) was significantly increased by AGE-BSA treatment,accompanied by RAGE overexpression.This augmentation can be reversed by RAGE knockdown.In addition, AGE-BSA activated ERK, P38, and JNK mitogen-activated protein kinases (MAPKs), which were supposed to participate in the regulation of Cx43.A MEK inhibitor PD98059, but not SB203580 (a p38 kinase inhibitor) or SP600125 (a JNK kinase inhibitor), abolished the effects of AGE-BSA on Cx43expression.Moreover, both Akt and PKC phosphorylation were time-dependently augmented by AGEBSA, PI3K inhibitor LY294002 (but not GF109203X, a PKC inhibitor) blocked the effects of AGE-BSA on Cx43 gap junctions.Taken together, AGE-BSA upregulated Cx43 expression via AGE-RAGE signaling,ERK MAPK and PI3K/Akt Signal transduction pathways appear to be involved in these processes.
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