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Icariin promotes angiogenic differentiation and prevents oxidative stress-induced autophagy in endothelial progenitor cells

Yubo Tang  Angela Jacobi  Corina Vater  Lijin Zou  Xuenong Zou  Maik Stiehler  
【摘要】:Reduced tissue levels of endothelial progenitor cells(EPCs) and functional impairment of endothelium are frequently observed in patients with diabetes and cardiovascular disease.The vascular endothelium is specifically sensitive to oxidative stress,and this is one of the mechanisms that causes widespread endothelial dysfunction in most cardiovascular diseases and disorders.Hence attention has increasingly been paid to enhance mobilization and differentiation of EPCs for therapeutic purposes.The aim of this study was to investigate whether Icariin,a natural bioactive component known from Traditional Chinese Medicine,can induce angiogenic differentiation and inhibit oxidative stress-induced cell dysfunction in bone marrow derived EPCs(BM-EPCs),and,if so,through what mechanisms.We observed that treatment of BM-EPCs with Icariin significantly promoted cell migration and capillary tube formation,substantially abrogated hydrogen peroxide(H2 O2)-induced apoptotic and autophagic programmed cell death that was linked to the reduced intracellular reactive oxygen species(ROS) levels and restored mitochondrial membrane potential(MMP).Icariin downregulated e NOS,as well as nicotinamide adenine dinucleotide phosphate-oxidase(NADPH) expression upon H2 O2 induction.These anti-apoptotic and anti-autophagic effects of Icariin are possibly mediated by restoring the loss of m TOR/p70 S6 K/4 EBP1 phosphorylation as well as attenuation of ATF2 and ERK1/2 protein levels after H2 O2 treatment.In summary,favourable modulation of the angiogenesis and redox states in BM-EPCs make Icariin a promising proangiogenic agent both enhancing vasculogenesis and protecting against endothelial dysfunction.Abbreviations:EPCs,endothelial progenitor cells;b FGF,basic fibroblast growth factor;ROS,reactive oxygen species;NADPH oxidase,nicotinamide adenine dinucleotide phosphate-oxidase;NO,nitric oxide;DCF,Dichloro-dihydro-fluorescein;MMP,mitochondrial membrane potential;NADPH oxidase,nicotinamide adenine dinucleotide phosphate-oxidase;DPI,diphenyliodonium;L-NAME,NG-nitro-L-arginine methyl ester;VEGF,vascular endothelial growth factor;KDR,kinase insert domain receptor;e NOS,endothelial nitric oxide synthase 3;VE-cadherin,vascular endothelial cadherin;v WF,von Willebrand factor;PECAM-1,platelet endothelial cell adhesion molecule;Nox4,NADPH oxidase 4;MAPK,mitogen activated protein kinase;m TOR,mammalian target of rapamycin;p70 S6 K,ribosomal protein S6 kinase;4 EBP1,eukaryotic translation Initiation Factor 4 E Binding Protein 1;ATF2,activating transcription factor 2;PARP,Poly(ADP-ribose) polymerase;SAPK/JNK,stress-activated protein kinase/Jun-amino-terminal kinase;3-MA,3-methy-ladenine.

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