Source:http://linkedlifedata.com/resource/pubmed/id/17513791
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
|
| pubmed:dateCreated |
2007-5-21
|
| pubmed:abstractText |
Angiopoietins 1 and 2 bind to Tie-2 expressed on endothelial cells and regulate vessel stabilization and angiogenesis. Tie-2(+) monocytes have been shown to be recruited to experimental tumors where they promote tumor angiogenesis. In this study, we show that 20% of CD14(+) human blood monocytes express Tie-2, and that these cells coexpress CD16 (FcgammaRIII) and are predominantly CD34 negative. Ang-2 is up-regulated by endothelial cells in malignant tumors and inflamed tissues, so our finding that Ang-2 is a chemoattractant for human Tie-2(+) monocytes and macrophages, suggests that it may help to recruit and regulate their distribution in such tissues. Ang-2 was also found to markedly inhibit release of the important proinflammatory cytokine, TNF-alpha, by monocytes in vitro. Following extravasation of monocytes, and their differentiation into macrophages, many accumulate in the hypoxic areas of inflamed and malignant tissues. Ang-2 is known to be up-regulated by hypoxia and we show that monocytes and macrophages up-regulate Tie-2 when exposed to hypoxia. Furthermore, hypoxia augmented the inhibitory effect of Ang-2 on the release of the anti-angiogenic cytokine, IL-12 by monocytes. In sum, our data indicate that Ang-2 may recruit Tie-2(+) monocytes to tumors and sites of inflammation, modulate their release of important cytokines and stimulate them to express a proangiogenic phenotype.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiopoietin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, TIE-2
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jun
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
178
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
7405-11
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:17513791-Angiopoietin-2,
pubmed-meshheading:17513791-Animals,
pubmed-meshheading:17513791-Cell Hypoxia,
pubmed-meshheading:17513791-Cell Membrane,
pubmed-meshheading:17513791-Cells, Cultured,
pubmed-meshheading:17513791-Chemotaxis, Leukocyte,
pubmed-meshheading:17513791-Cytokines,
pubmed-meshheading:17513791-Gene Expression Regulation,
pubmed-meshheading:17513791-Granulocytes,
pubmed-meshheading:17513791-Humans,
pubmed-meshheading:17513791-Inflammation Mediators,
pubmed-meshheading:17513791-Lymphocyte Subsets,
pubmed-meshheading:17513791-Macrophages,
pubmed-meshheading:17513791-Mice,
pubmed-meshheading:17513791-Monocytes,
pubmed-meshheading:17513791-Neoplasms, Experimental,
pubmed-meshheading:17513791-Neovascularization, Pathologic,
pubmed-meshheading:17513791-RNA, Messenger,
pubmed-meshheading:17513791-Receptor, TIE-2,
pubmed-meshheading:17513791-Up-Regulation
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| pubmed:year |
2007
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| pubmed:articleTitle |
Expression of Tie-2 by human monocytes and their responses to angiopoietin-2.
|
| pubmed:affiliation |
Tumor Targeting Group, Academic Unit of Pathology, Division of Genomic Medicine, The Sir Henry Wellcome Laboratories for Medical Research, University of Sheffield Medical School, Sheffield, United Kingdom.
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| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|