pubmed-article:16894355 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C0007581 | lld:lifeskim |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C0002199 | lld:lifeskim |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C0332157 | lld:lifeskim |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C0549178 | lld:lifeskim |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:16894355 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
pubmed-article:16894355 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:16894355 | pubmed:dateCreated | 2006-9-19 | lld:pubmed |
pubmed-article:16894355 | pubmed:abstractText | Although the antiangiogenic activity of type I interferons (IFN) is well known, the mechanism by which it occurs is unclear. In the present study, we have investigated effects of short-term and long-term IFN-alpha exposure on different types of endothelial cells (EC). Short-term IFN-alpha treatment resulted in a distinct reduction of apoptosis of serum and growth factor starved HUVEC and HDMEC. This was accompanied by a strong upregulation of the IFN inducible guanylate binding protein-1 (GBP-1) whereas no consistent regulation of several known antiapoptotic proteins was evident. Stable transfection of HUVEC with an expression vector for GBP-1 mimicked the protective effect of IFN-alpha, suggesting that GBP-1 may contribute to the inhibition of apoptosis. When IFN-alpha, together with serum and EC growth factors, was present continuously a decrease of population doublings by more than 40% was observed in both HDMEC and HCAEC. In addition, the cells displayed a senescent phenotype significantly earlier than control cells and showed an increased adherence for monocytes. Our findings suggest that the antiangiogenic effect of IFN-alpha is mediated by inducing EC senescence rather than EC apoptosis. Furthermore IFN-alpha released in chronic inflammatory conditions might contribute via its prosenescent activity to the pathogenesis of atherosclerosis. | lld:pubmed |
pubmed-article:16894355 | pubmed:language | eng | lld:pubmed |
pubmed-article:16894355 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16894355 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16894355 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16894355 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16894355 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16894355 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16894355 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16894355 | pubmed:month | Oct | lld:pubmed |
pubmed-article:16894355 | pubmed:issn | 0023-6837 | lld:pubmed |
pubmed-article:16894355 | pubmed:author | pubmed-author:TschachlerErw... | lld:pubmed |
pubmed-article:16894355 | pubmed:author | pubmed-author:BirnerPeterP | lld:pubmed |
pubmed-article:16894355 | pubmed:author | pubmed-author:PammerJohanne... | lld:pubmed |
pubmed-article:16894355 | pubmed:author | pubmed-author:ReinischChris... | lld:pubmed |
pubmed-article:16894355 | pubmed:author | pubmed-author:PogodaKristin... | lld:pubmed |
pubmed-article:16894355 | pubmed:author | pubmed-author:SturzlMichael... | lld:pubmed |
pubmed-article:16894355 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16894355 | pubmed:volume | 86 | lld:pubmed |
pubmed-article:16894355 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16894355 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16894355 | pubmed:pagination | 997-1007 | lld:pubmed |
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pubmed-article:16894355 | pubmed:meshHeading | pubmed-meshheading:16894355... | lld:pubmed |
pubmed-article:16894355 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16894355 | pubmed:articleTitle | Interferon-alpha prevents apoptosis of endothelial cells after short-term exposure but induces replicative senescence after continuous stimulation. | lld:pubmed |
pubmed-article:16894355 | pubmed:affiliation | Institute of Clinical Pathology, Medical University of Vienna, Vienna, Austria. | lld:pubmed |
pubmed-article:16894355 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16894355 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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