Palmitic acid promotes endothelial progenitor cells apoptosis via p38 and JNK mitogen-activated protein kinase pathways(Abstract)
Objective Recent studies have demonstrated that palmitic acid(PA) could regulate endothelial progenitor cells(EPCs) function(migration,proliferation,survival and angiogenesis) via various signal pathways,but the effect of PA on EPCs apoptosis and associated mechanisms are still elusive.Methods The human EPCs were oltained by Ficoll density gradient centrifugation and cultured in M199 medium containing rh-VEGF(30 ng/ml),rh-b-FGF(6 ng/ml) and 10％ fetal bovine serum for 7 days.The adhesive EPCs were harvested,then challenged with different concentrations of PA(ranging from 0 to 800 μmol/L) for 48 h and 400 μmol/L PA for different time periods(ranging from 0 to 60 h) after 12 h synchronization with serum free medium.The EPCs apoptosis was determined by flow cytometry,expression of caspase3,phosphorylated ERK1/2,JNK and p38 mitogen-activated protein kinase(MAPK) were quantified by Western-blot.The effect of PA on caspase-3 activity in the absence or presence of specific MAPK pathway inhibitors was determined by colorimetry.Results PA increased EPCs apoptosis in a dose-and time-dependent manner,upregulated phosphorylated p38 and JNK,caspase-3 expression of EPCs while ERK expression was not affected.PA induced EPCs apoptosis could be partly ameliorated by p38 inhibitor SB203580 and JNK inhibitor SP600125,but not by ERK1/2 inhibitor PD98059.Conclusion These findings suggested that PA promoted EPCs apoptosis via p38 and JNK MAPKs pathways.
Endothelial progenitor cells Palmitic acid Apoptosis Mitogen-activated protein kinase
Hai-long JIANG Mei LI Zong-gui WU Chun LIANG
Department of Cardiology,Second Hospital Affiliated to the Second Military Medical University,Shangh Department of Cardiology,Second Hospital Affiliated to the Second Military Medical University,Shangh
国内会议
广州
英文
67-67
2009-11-01（万方平台首次上网日期，不代表论文的发表时间）