【摘 要】
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Objective Advanced glycation end products(AGEs) and endothelial progenitor cells(EPCs) play divergent roles in the process of atherosclerosis.We investigated the effects of AGE-human serum albumin(AGE
【机 构】
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Department of Cardiology,Second Hospital Affiliated to the Second Military Medical University,Shangh
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Objective Advanced glycation end products(AGEs) and endothelial progenitor cells(EPCs) play divergent roles in the process of atherosclerosis.We investigated the effects of AGE-human serum albumin(AGE-HSA) on receptor expression for AGEs(RAGE) and EPCs apoptosis.Methods The human mononuclear cellswere obtained by Ficoll density gradient centrifugation and cultured in M199 medium containing rh-VEGF(30 ng/ml),rh-b-FGF(6 ng/ml) and 20％ NBCS for 8 days.The adhesive EPCs were sequentially harvested after 24 hourssynchronization and challenged with AGE-HSA(concentration range from 0 to 300 μg/ml) for 24 hours and 200 μg/ml AGE-HSA(time range from 0 to 36 hours).EPCs apoptosis and migration were determined,expressions of RAGE,phosphorylated ERK1/2,JNK and p38 mitogen-activated protein kinase(MAPK) of EPCs were quantified by fluorescent quantitation RT-PCR and Western-blot while effect of AGE-HSA on NF-κB activtiy was determined by EMSA(electrophoretic mobility shift assay) in the presence and absence of special MAPK pathways pathway inhibitors.Results AGE-HSA upregulated the expression of RAGE,this effect could be significantly inhibited by p38 MAPK and ERK MAPK inhibitor,but not by JNK MAPK inhibitor.AGE-HSA also promoted EPCs apoptosis and inhibited EPCs migration via the activation of NF-κB,these effects could be significantly attenuated by the anti-RAGE neutralizing antibody as well as by p38 and ERK MAPK inhibitors.Conclusion AGE-HSA could promote atherosclerosis by upregulating EPCs RAGE expressions and promoting EPCs apoptosis via p38,ERK MAPK pathways and activation of NF-κB.
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