Source:http://linkedlifedata.com/resource/pubmed/id/17704650
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2007-8-20
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pubmed:abstractText |
Trichostatin A and helixor A increased thrombospondin-1 expression by ECV304 cells at both mRNA and protein levels by transcriptional activation through the enhancement of tsp-1 promoter activity. The induction of thrombospondin-1 by these agents potently reduced ECV 304 cell migration and capillary-like tube formation on Matrigel; these findings were confirmed by the neutralization of thrombospondin-1 using a specific antibody. In the presence of exogenous vascular endothelial growth factor, however, these agents had a different effect on the vascular endothelial growth factor-induced tube formation; trichostatin A remarkably inhibited tube formation regardless of the presence of exogenous vascular endothelial growth factor, whereas helixor A reduced it to 70-80% of the control level. Interestingly, when the helixor A-generated conditioned media were concentrated three-fold and the endogenous vascular endothelial growth factor was removed, tube formation was remarkably inhibited compared with the effect of three-fold concentrated conditioned media that had endogenous vascular endothelial growth factor. Additionally, in media with endogenous vascular endothelial growth factor that were concentrated five-fold, tube formation was markedly blocked regardless of the presence of exogenous or endogenous vascular endothelial growth factor. Thus, our results indicate that trichostatin A-induced or helixor A-induced antiangiogenesis is mediated by both agents; increased, absolute and relative levels of thrombospondin-1 to the vascular endothelial growth factor level are critical in angiogenesis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiogenesis Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Conditioned,
http://linkedlifedata.com/resource/pubmed/chemical/Helixor,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxamic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Plant Extracts,
http://linkedlifedata.com/resource/pubmed/chemical/Thrombospondin 1,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/trichostatin A
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0959-4973
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
18
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1005-14
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pubmed:meshHeading |
pubmed-meshheading:17704650-Angiogenesis Inhibitors,
pubmed-meshheading:17704650-Cell Line,
pubmed-meshheading:17704650-Cell Movement,
pubmed-meshheading:17704650-Cell Survival,
pubmed-meshheading:17704650-Culture Media, Conditioned,
pubmed-meshheading:17704650-Dose-Response Relationship, Drug,
pubmed-meshheading:17704650-Endothelial Cells,
pubmed-meshheading:17704650-Humans,
pubmed-meshheading:17704650-Hydroxamic Acids,
pubmed-meshheading:17704650-Neovascularization, Pathologic,
pubmed-meshheading:17704650-Plant Extracts,
pubmed-meshheading:17704650-Thrombospondin 1,
pubmed-meshheading:17704650-Up-Regulation,
pubmed-meshheading:17704650-Vascular Endothelial Growth Factors
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pubmed:year |
2007
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pubmed:articleTitle |
Differential regulation of thrombospondin-1 expression and antiangiogenesis of ECV304 cells by trichostatin A and helixor A.
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pubmed:affiliation |
Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
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pubmed:publicationType |
Journal Article
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