Source:http://linkedlifedata.com/resource/pubmed/id/17293480
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2007-3-16
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pubmed:abstractText |
We have recently demonstrated that endogenous erythropoietin (Epo)/Epo receptor (EpoR) system plays an important protective role in hypoxia-induced pulmonary hypertension. However, it remains to be examined whether vascular EpoR system contributes to angiogenesis in response to ischemia. We examined angiogenesis in EpoR(-/-)-rescued mice that lack EpoR in most organs including cardiovascular system except erythroid-lineage cells. Two weeks after femoral artery ligation, blood flow recovery, activation of VEGF/VEGF receptor system, and mobilization of endothelial progenitor cells were all impaired in EpoR(-/-)-rescued mice as compared with wild-type (WT) mice. Bone marrow (BM) transplantation with WT-BM cells in EpoR(-/-)-rescued mice partially but significantly improved blood flow recovery after hindlimb ischemia. The extent of VEGF upregulation and the number of BM-derived cells in ischemic tissue were significantly less in EpoR(-/-)-rescued mice compared with WT mice even after BM reconstitution with WT-BM cells. Similarly, the recovery of blood flow was significantly impaired in recipient EpoR(-/-)-rescued mice that had been transplanted with WT-BM or EpoR(-/-)-rescued-BM as compared with recipient WT mice. Furthermore, the Matrigel implantation assay and aortic ring assay showed that microvessel growth in vitro was significantly reduced in EpoR(-/-)-rescued mice as compared with WT mice. These results indicate that vascular EpoR system also plays an important role in angiogenesis in response to hindlimb ischemia through upregulation of VEGF/VEGF receptor system, both directly by enhancing neovascularization and indirectly by recruiting endothelial progenitor cells and BM-derived proangiogenic cells.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1524-4571
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
16
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pubmed:volume |
100
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
662-9
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pubmed:meshHeading |
pubmed-meshheading:17293480-Animals,
pubmed-meshheading:17293480-Cell Movement,
pubmed-meshheading:17293480-Endothelium, Vascular,
pubmed-meshheading:17293480-Hindlimb,
pubmed-meshheading:17293480-Humans,
pubmed-meshheading:17293480-Ischemia,
pubmed-meshheading:17293480-Male,
pubmed-meshheading:17293480-Mice,
pubmed-meshheading:17293480-Mice, Inbred C57BL,
pubmed-meshheading:17293480-Mice, Knockout,
pubmed-meshheading:17293480-Mice, Transgenic,
pubmed-meshheading:17293480-Neovascularization, Pathologic,
pubmed-meshheading:17293480-Receptors, Erythropoietin,
pubmed-meshheading:17293480-Stem Cells,
pubmed-meshheading:17293480-Up-Regulation,
pubmed-meshheading:17293480-Vascular Endothelial Growth Factor A
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pubmed:year |
2007
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pubmed:articleTitle |
Important role of erythropoietin receptor to promote VEGF expression and angiogenesis in peripheral ischemia in mice.
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pubmed:affiliation |
Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan. fukumoto@cardio.med.tohoku.ac.jp.
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pubmed:publicationType |
Journal Article,
Comparative Study
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