| pubmed-article:21435467 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21435467 | lifeskim:mentions | umls-concept:C0302600 | lld:lifeskim |
| pubmed-article:21435467 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:21435467 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
| pubmed-article:21435467 | lifeskim:mentions | umls-concept:C0332448 | lld:lifeskim |
| pubmed-article:21435467 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:21435467 | pubmed:dateCreated | 2011-3-25 | lld:pubmed |
| pubmed-article:21435467 | pubmed:abstractText | Vascular adhesion protein-1 (VAP-1) contributes to inflammatory and angiogenic diseases, including cancer and age-related macular degeneration. It is expressed in blood vessels and contributes to inflammatory leukocyte recruitment. The cytokines IL-1? and vascular endothelial growth factor A (VEGF-A) modulate angiogenesis, lymphangiogenesis, and leukocyte infiltration. The lymphatic endothelium expresses intercellular adhesion molecule-1 and vascular adhesion molecule-1, which facilitate leukocyte transmigration into the lymphatic vessels. However, whether lymphatics express VAP-1 and whether they contribute to cytokine-dependent lymph- and angiogenesis are unknown. We investigated the role of VAP-1 in IL-1?- and VEGF-A-induced lymph- and angiogenesis using the established corneal micropocket assay. IL-1? increased VAP-1 expression in the inflamed cornea. Our in vivo molecular imaging revealed significantly higher VAP-1 expression in neovasculature than in the preexisting vessels. VAP-1 was expressed in blood but not lymphatic vessels in vivo. IL-1?-induced M2 macrophage infiltration and lymph- and angiogenesis were blocked by VAP-1 inhibition. In contrast, VEGF-A-induced lymph- and angiogenesis were unaffected by VAP-1 inhibition. Our results indicate a key role for VAP-1 in lymph- and angiogenesis-related macrophage recruitment. VAP-1 might become a new target for treatment of inflammatory lymph- and angiogenic diseases, including cancer. | lld:pubmed |
| pubmed-article:21435467 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21435467 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21435467 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21435467 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:21435467 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:21435467 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21435467 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21435467 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:21435467 | pubmed:issn | 1525-2191 | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:MashimaYukihi... | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:SunDaweiD | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:Hafezi-Moghad... | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:NodaKousukeK | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:NakaoShintaro... | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:XieFangF | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:MahdiTaherT | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:ZandiSouskaS | lld:pubmed |
| pubmed-article:21435467 | pubmed:author | pubmed-author:ScheringAlexa... | lld:pubmed |
| pubmed-article:21435467 | pubmed:copyrightInfo | Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:21435467 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21435467 | pubmed:volume | 178 | lld:pubmed |
| pubmed-article:21435467 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21435467 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21435467 | pubmed:pagination | 1913-21 | lld:pubmed |
| pubmed-article:21435467 | pubmed:dateRevised | 2011-8-16 | lld:pubmed |
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| pubmed-article:21435467 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21435467 | pubmed:articleTitle | VAP-1-mediated M2 macrophage infiltration underlies IL-1?- but not VEGF-A-induced lymph- and angiogenesis. | lld:pubmed |
| pubmed-article:21435467 | pubmed:affiliation | Angiogenesis Laboratory, Massachusetts Eye & Ear Infirmary, Boston, MA 02115, USA. | lld:pubmed |
| pubmed-article:21435467 | pubmed:publicationType | Journal Article | lld:pubmed |
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