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rdf:type |
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lifeskim:mentions |
umls-concept:C0009491,
umls-concept:C0043240,
umls-concept:C0205307,
umls-concept:C0206364,
umls-concept:C0221099,
umls-concept:C0221912,
umls-concept:C0374711,
umls-concept:C0533670,
umls-concept:C0851285,
umls-concept:C1579762,
umls-concept:C1705181
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pubmed:issue |
3
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pubmed:dateCreated |
2001-4-19
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pubmed:abstractText |
It has become evident that a closely regulated presence of vascular endothelial growth factor (VEGF) and angiopoietin (Ang) factors determines the fate of blood vessel formation during angiogenesis. As angiogenesis is central to a normal wound-healing process, we investigated the regulation of Ang-1 and -2 and the related tyrosine kinase with immunoglobulin and epidermal growth factor homology (Tie)-1 and -2 receptors during normal repair in Balb/c mice and diabetes-impaired wound healing conditions in genetically diabetic (db/db) mice. For both normal and impaired healing conditions, we observed a constitutive expression of Ang-1, which was paralleled by an increase of Ang-2 upon injury. Whereas the observed Ang-2 expression declines from Day 7 after injury in control mice, diabetic-impaired healing was characterized by still increasing amounts of Ang-2 at these time points. Furthermore, Tie-1 was strongly induced during repair with a prolonged expression in diabetic mice, whereas Tie-2 expression was constitutive during normal repair but completely absent in diabetes-impaired healing. The overexpression of Ang-2 in the presence of markedly reduced VEGF in wounds of diabetic mice was associated with a dramatic decrease in endothelial cell numbers compared with normal healing as assessed by analysis of the endothelium-specific markers CD31 and von Willebrand factor, whereas the lymphatic endothelium remained stable as determined by expression of VEGF receptor-3 (VEGFR-3/Flt-4).
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiopoietin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Angiopoietin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Angpt1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelial Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, TIE-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, TIE-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, TIE,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0023-6837
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
81
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
361-73
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pubmed:dateRevised |
2011-8-3
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pubmed:meshHeading |
pubmed-meshheading:11310829-Angiopoietin-1,
pubmed-meshheading:11310829-Angiopoietin-2,
pubmed-meshheading:11310829-Animals,
pubmed-meshheading:11310829-Diabetes Mellitus, Type 2,
pubmed-meshheading:11310829-Endothelial Growth Factors,
pubmed-meshheading:11310829-Endothelium, Vascular,
pubmed-meshheading:11310829-Fascia,
pubmed-meshheading:11310829-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:11310829-Lymphatic System,
pubmed-meshheading:11310829-Lymphokines,
pubmed-meshheading:11310829-Membrane Glycoproteins,
pubmed-meshheading:11310829-Mice,
pubmed-meshheading:11310829-Mice, Inbred BALB C,
pubmed-meshheading:11310829-Mice, Inbred C57BL,
pubmed-meshheading:11310829-Mice, Mutant Strains,
pubmed-meshheading:11310829-Muscle, Smooth,
pubmed-meshheading:11310829-Proteins,
pubmed-meshheading:11310829-RNA, Messenger,
pubmed-meshheading:11310829-Receptor, TIE-1,
pubmed-meshheading:11310829-Receptor, TIE-2,
pubmed-meshheading:11310829-Receptor Protein-Tyrosine Kinases,
pubmed-meshheading:11310829-Receptors, Cell Surface,
pubmed-meshheading:11310829-Receptors, TIE,
pubmed-meshheading:11310829-Skin,
pubmed-meshheading:11310829-Vascular Endothelial Growth Factor A,
pubmed-meshheading:11310829-Vascular Endothelial Growth Factors,
pubmed-meshheading:11310829-Wound Healing
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pubmed:year |
2001
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pubmed:articleTitle |
Expressional regulation of angiopoietin-1 and -2 and the tie-1 and -2 receptor tyrosine kinases during cutaneous wound healing: a comparative study of normal and impaired repair.
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pubmed:affiliation |
Zentrum der Pharmakologie, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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