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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2006-6-9
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pubmed:abstractText |
We investigated whether the mobilization of endothelial progenitor cells (EPCs) by exogenous erythropoietin (Epo) promotes the repair of injured endothelium. Recombinant human Epo was injected (1000 IU/kg for the initial 3 days) after wire injury of the femoral artery of mice. Neointimal formation was inhibited by Epo to 48% of the control (P<0.05) in an NO-dependent manner. Epo induced a 1.4-fold increase in reendothelialized area of day 14 denuded vessels, 55% of which was derived from bone marrow (BM) cells. Epo increased the circulating Sca-1(+)/Flk-1(+) EPCs (2.0-fold, P<0.05) with endothelial properties NO dependently. BM replacement by GFP- or beta-galactosidase-overexpressing cells showed that Epo stimulated both differentiation of BM-derived EPCs and proliferation of resident ECs. BM-derived ECs increased 2.2- to 2.7-fold (P<0.05) in the Epo-induced neoendothelium, where the expression of Epo receptor was upregulated. Epo induced Akt/eNOS phosphorylation and NO synthesis on EPCs and exerted an antiapoptotic action on wire-injured arteries. In conclusion, Epo treatment inhibits the neointimal hyperplasia after arterial injury in an NO-dependent manner by acting on the injured vessels and mobilizing EPCs to the neo-endothelium.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1524-4571
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pubmed:author |
pubmed-author:AadachiYasushiY,
pubmed-author:MatsubaraHiroakiH,
pubmed-author:MatsuiAkihiroA,
pubmed-author:MatsunagaShinsakuS,
pubmed-author:MatsunoKuniharuK,
pubmed-author:NomuraTetsuyaT,
pubmed-author:OkigakiMitsuhikoM,
pubmed-author:TakahashiTomosaburoT,
pubmed-author:TateishiKentoK,
pubmed-author:TatsumiTetsuyaT,
pubmed-author:UraoNorifumiN,
pubmed-author:YamadaHiroyukiH
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pubmed:issnType |
Electronic
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pubmed:day |
9
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pubmed:volume |
98
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1405-13
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:16645141-Animals,
pubmed-meshheading:16645141-Apoptosis,
pubmed-meshheading:16645141-Bone Marrow Cells,
pubmed-meshheading:16645141-Bone Marrow Transplantation,
pubmed-meshheading:16645141-Cell Movement,
pubmed-meshheading:16645141-Cells, Cultured,
pubmed-meshheading:16645141-Endothelium, Vascular,
pubmed-meshheading:16645141-Enzyme Activation,
pubmed-meshheading:16645141-Erythropoietin,
pubmed-meshheading:16645141-Femoral Artery,
pubmed-meshheading:16645141-Humans,
pubmed-meshheading:16645141-Hyperplasia,
pubmed-meshheading:16645141-Male,
pubmed-meshheading:16645141-Mice,
pubmed-meshheading:16645141-Mice, Inbred C57BL,
pubmed-meshheading:16645141-Nitric Oxide,
pubmed-meshheading:16645141-Nitric Oxide Synthase Type III,
pubmed-meshheading:16645141-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:16645141-Receptors, Erythropoietin,
pubmed-meshheading:16645141-Recombinant Proteins,
pubmed-meshheading:16645141-Tunica Intima,
pubmed-meshheading:16645141-Wound Healing,
pubmed-meshheading:16645141-Wounds and Injuries
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pubmed:year |
2006
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pubmed:articleTitle |
Erythropoietin-mobilized endothelial progenitors enhance reendothelialization via Akt-endothelial nitric oxide synthase activation and prevent neointimal hyperplasia.
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pubmed:affiliation |
Department of Cardiovascular Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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