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Advanced Glycation End Products Upregulates The Expression Of Connexin 43 Via ERK MAPK And PI3K/Akt Pathways In Human Endothelial Cells

Advanced Glycation End Products Upregulates The Expression O...

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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

作者： yanbo zhao shengjie xu chongying jin guosheng fu shaoxiang weng

＜正＞Intercellular communication through gap junctions plays an essential role in maintaining the functional integrity of vascular *** emerging evidence suggests that advanced glycation end products（AGEs） may impair endothelial ***,its effect on connexin43 （Cx43） gap junction in endothelial cells remains *** we investigated the effect Of AGEbovine serum albumin（AGE-BSA） on Cx43 gap junction in endothelial *** levels of Cx43 protein in human umbilical vein endothelial cells（HUVECs） was significantly increased by AGE-BSA treatment, accompanied by RAGE *** augmentation can be reversed by RAGE *** 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 Cx43 ***,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 *** 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.

关键词： advanced glycation end products endothelial cells connexin43 gap junction

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Leptin protects rat cardiomyocytes against TNF-α-induced apoptosis

Leptin protects rat cardiomyocytes against TNF-α-induced ap...

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2014年浙江省心电生理与起搏学术年会

作者： Lu Yu yanbo zhao shengjie,xu chongying jin Min Wang guosheng fu Department of Cardiovascular Medicine Sir Run Run Shaw HospitalCollege of MedicineZhejiang University

Aims:Leptin,an important adipose-derived hormone,is recognized as a crucial protein in *** studies indicated that leptin is associated with cardiac pathophysiology,however,the role and the mechanism of leptin in cardiomyocyte apoptosis is poorly understood,In this study,we investigated whether leptin exerted protective effect on cardiomyocytes exposed to tumor necrosis factor-alpha(TNF-α)and the possible ***:Neonatal rat cardiomyocytes were subjected to TNF-α(10ng/ml for 24h)in the presence or absence of leptin(10nM).Apoptosis was analyzed by FITC/Annexin-V flow cytometry,as well as cleaved caspase-3/PARP and cytochrome C/*** Mitogen-activated protein kinases(MAPK)and NF-κB were quantified by Western ***:Increased annexin-V binding and cleaved caspase-3/PARP were found in cardiomyocytes exposed to TNF-α,and they were attenuated by leptin *** also protected cardiomyocytes against mitochondrial apoptosis by inhibiting elevated cytochrome C and improving decreased *** pretreatment inhibited TNF-α-induced P38 and NF-κB *** p38 MAPK inhibitor and NF-κB inhibitor,however,attenuated the protective effect of ***:Leptin might have anti-apoptotic effect in cardiomyocytes exposed to TNF-αby inhibiting TNF-α-activated p38 MAPK and NF-κB pathways.

关键词： Leptin-TNF-α-Apoptosis-Cardiomyocytes

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