| pubmed-article:15855638 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15855638 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:15855638 | lifeskim:mentions | umls-concept:C1333569 | lld:lifeskim |
| pubmed-article:15855638 | lifeskim:mentions | umls-concept:C0010031 | lld:lifeskim |
| pubmed-article:15855638 | lifeskim:mentions | umls-concept:C1257789 | lld:lifeskim |
| pubmed-article:15855638 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:15855638 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:15855638 | lifeskim:mentions | umls-concept:C0205359 | lld:lifeskim |
| pubmed-article:15855638 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:15855638 | pubmed:dateCreated | 2005-4-27 | lld:pubmed |
| pubmed-article:15855638 | pubmed:abstractText | Lymphangiogenesis, the formation of new lymphatic vessels, is important for tumor metastasis and induction of immunity to peripheral antigens including organ transplants. We herein describe a novel mouse model of spontaneous, secondary lymphangiogenesis in the normally avascular cornea. corn1 mice, which suffer from a deletion in the gene encoding the cytoskeletal protein destrin, develop hemangiogenesis as well as spontaneous outgrowth of LYVE-1+++/CD31+ lymphatic vessels into the cornea starting at age 4 weeks. Corneal lymphangiogenesis is delayed in onset, is less intense, and regresses earlier compared with hemangiogenesis. Moreover, the lymphangiogenesis is preceded only by a mild recruitment of CD45+ inflammatory cells into the cornea. In contrast to mice with inflammation-induced hem- and lymphangiogenesis, corn1 mice do not develop breakdown of the blood-aqueous barrier. Finally, in this novel mouse model, a blocking anti-VEGFR3 antibody significantly inhibited not only lymph- but also hemangiogenesis. In summary, destrin deletion has differential effects on spontaneous hem- and lymphangiogenesis in the normally avascular cornea and represents a novel mouse model to study the mechanisms of lymphangiogenesis and to test the antihem- and antilymphangiogenic properties of known or new antiangiogenic agents. | lld:pubmed |
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| pubmed-article:15855638 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15855638 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15855638 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:15855638 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15855638 | pubmed:month | May | lld:pubmed |
| pubmed-article:15855638 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:JacksonDavidD | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:SmithRichard... | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:KruseFriedric... | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:IkedaAkihiroA | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:NishinaPatsy... | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:DanaM RezaMR | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:ChenLuL | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:StreileinJ... | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:CursiefenClau... | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:IkedaSakaeS | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:MoJun-SongJS | lld:pubmed |
| pubmed-article:15855638 | pubmed:author | pubmed-author:PytowskiBroni... | lld:pubmed |
| pubmed-article:15855638 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15855638 | pubmed:volume | 166 | lld:pubmed |
| pubmed-article:15855638 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15855638 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15855638 | pubmed:pagination | 1367-77 | lld:pubmed |
| pubmed-article:15855638 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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