pubmed-article:18417479 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18417479 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
pubmed-article:18417479 | lifeskim:mentions | umls-concept:C0206364 | lld:lifeskim |
pubmed-article:18417479 | lifeskim:mentions | umls-concept:C0754090 | lld:lifeskim |
pubmed-article:18417479 | lifeskim:mentions | umls-concept:C1159441 | lld:lifeskim |
pubmed-article:18417479 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
pubmed-article:18417479 | pubmed:issue | 23 | lld:pubmed |
pubmed-article:18417479 | pubmed:dateCreated | 2008-6-2 | lld:pubmed |
pubmed-article:18417479 | pubmed:abstractText | MicroRNAs (miRNAs) are small non-protein-coding RNAs that function as negative gene expression regulators. In the present study, we investigated miRNAs role in endothelial cell response to hypoxia. We found that the expression of miR-210 progressively increased upon exposure to hypoxia. miR-210 overexpression in normoxic endothelial cells stimulated the formation of capillary-like structures on Matrigel and vascular endothelial growth factor-driven cell migration. Conversely, miR-210 blockade via anti-miRNA transfection inhibited the formation of capillary-like structures stimulated by hypoxia and decreased cell migration in response to vascular endothelial growth factor. miR-210 overexpression did not affect endothelial cell growth in both normoxia and hypoxia. However, anti-miR-210 transfection inhibited cell growth and induced apoptosis, in both normoxia and hypoxia. We determined that one relevant target of miR-210 in hypoxia was Ephrin-A3 since miR-210 was necessary and sufficient to down-modulate its expression. Moreover, luciferase reporter assays showed that Ephrin-A3 was a direct target of miR-210. Ephrin-A3 modulation by miR-210 had significant functional consequences; indeed, the expression of an Ephrin-A3 allele that is not targeted by miR-210 prevented miR-210-mediated stimulation of both tubulogenesis and chemotaxis. We conclude that miR-210 up-regulation is a crucial element of endothelial cell response to hypoxia, affecting cell survival, migration, and differentiation. | lld:pubmed |
pubmed-article:18417479 | pubmed:language | eng | lld:pubmed |
pubmed-article:18417479 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18417479 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:18417479 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18417479 | pubmed:month | Jun | lld:pubmed |
pubmed-article:18417479 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:18417479 | pubmed:author | pubmed-author:CapogrossiMau... | lld:pubmed |
pubmed-article:18417479 | pubmed:author | pubmed-author:PompilioGiuli... | lld:pubmed |
pubmed-article:18417479 | pubmed:author | pubmed-author:MartelliFabio... | lld:pubmed |
pubmed-article:18417479 | pubmed:author | pubmed-author:FasanaroPasqu... | lld:pubmed |
pubmed-article:18417479 | pubmed:author | pubmed-author:Di... | lld:pubmed |
pubmed-article:18417479 | pubmed:author | pubmed-author:D'AlessandraY... | lld:pubmed |
pubmed-article:18417479 | pubmed:author | pubmed-author:MelchionnaRob... | lld:pubmed |
pubmed-article:18417479 | pubmed:author | pubmed-author:RomaniSvevaS | lld:pubmed |
pubmed-article:18417479 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:18417479 | pubmed:day | 6 | lld:pubmed |
pubmed-article:18417479 | pubmed:volume | 283 | lld:pubmed |
pubmed-article:18417479 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18417479 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18417479 | pubmed:pagination | 15878-83 | lld:pubmed |
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pubmed-article:18417479 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18417479 | pubmed:articleTitle | MicroRNA-210 modulates endothelial cell response to hypoxia and inhibits the receptor tyrosine kinase ligand Ephrin-A3. | lld:pubmed |
pubmed-article:18417479 | pubmed:affiliation | Laboratorio di Patologia Vascolare, Istituto Dermopatico dell'Immacolata, IRCCS, 00167 Rome. | lld:pubmed |
pubmed-article:18417479 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18417479 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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