| pubmed-article:17101841 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17101841 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:17101841 | lifeskim:mentions | umls-concept:C0033384 | lld:lifeskim |
| pubmed-article:17101841 | lifeskim:mentions | umls-concept:C1514562 | lld:lifeskim |
| pubmed-article:17101841 | lifeskim:mentions | umls-concept:C1883221 | lld:lifeskim |
| pubmed-article:17101841 | lifeskim:mentions | umls-concept:C1655807 | lld:lifeskim |
| pubmed-article:17101841 | lifeskim:mentions | umls-concept:C1883204 | lld:lifeskim |
| pubmed-article:17101841 | lifeskim:mentions | umls-concept:C1880389 | lld:lifeskim |
| pubmed-article:17101841 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17101841 | pubmed:dateCreated | 2006-12-22 | lld:pubmed |
| pubmed-article:17101841 | pubmed:abstractText | Prolyl hydroxylase domain 2 protein (PHD2) signals the degradation of hypoxia-inducible factor (HIF)-1alpha by hydroxylating specific prolyl residues located within oxygen-dependent degradation domains. As expected, endothelial cells (ECs) overexpressing PHD2 had reduced HIF-1alpha and vascular endothelial growth factor-A expression and failed to accelerate their proliferation in response to hypoxia. Surprisingly, although these cells displayed further reductions in HIF-1alpha and vascular endothelial growth factor-A expression when cultured under normoxia, there was no further reduction in EC proliferation. Thus, there seemed to be no consistent correlation between PHD2 hydroxylase-mediated suppression of HIF-1alpha expression and inhibition of EC growth. Indeed, overexpression of a mutant PHD2 lacking hydroxylase activity also greatly diminished EC response to hypoxia-induced increase in proliferation, in spite of the fact that hypoxia-induced HIF-1alpha accumulation was not affected by mutant PHD2. These data strongly suggest the existence of a hydroxylase-independent mechanism for PHD2-mediated inhibition of EC proliferation under hypoxia. In support of a physiological relevance of PHD2 overexpression, we found that endogenous PHD2 expression was significantly upregulated by hypoxia and that silencing of the Phd2 gene by RNA interference significantly enhanced hypoxia-induced EC proliferation. In conclusion, this study demonstrates that PHD2 may act as a negative feedback regulator to antagonize hypoxia-induced EC proliferation. | lld:pubmed |
| pubmed-article:17101841 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17101841 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17101841 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17101841 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17101841 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17101841 | pubmed:issn | 1524-4563 | lld:pubmed |
| pubmed-article:17101841 | pubmed:author | pubmed-author:FongGuo-HuaGH | lld:pubmed |
| pubmed-article:17101841 | pubmed:author | pubmed-author:TakedaKotaroK | lld:pubmed |
| pubmed-article:17101841 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:17101841 | pubmed:volume | 49 | lld:pubmed |
| pubmed-article:17101841 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17101841 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17101841 | pubmed:pagination | 178-84 | lld:pubmed |
| pubmed-article:17101841 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:17101841 | pubmed:meshHeading | pubmed-meshheading:17101841... | lld:pubmed |
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| pubmed-article:17101841 | pubmed:meshHeading | pubmed-meshheading:17101841... | lld:pubmed |
| pubmed-article:17101841 | pubmed:meshHeading | pubmed-meshheading:17101841... | lld:pubmed |
| pubmed-article:17101841 | pubmed:meshHeading | pubmed-meshheading:17101841... | lld:pubmed |
| pubmed-article:17101841 | pubmed:meshHeading | pubmed-meshheading:17101841... | lld:pubmed |
| pubmed-article:17101841 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17101841 | pubmed:articleTitle | Prolyl hydroxylase domain 2 protein suppresses hypoxia-induced endothelial cell proliferation. | lld:pubmed |
| pubmed-article:17101841 | pubmed:affiliation | Center for Vascular Biology, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06030-3501, USA. | lld:pubmed |
| pubmed-article:17101841 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17101841 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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