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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2001-5-2
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pubmed:abstractText |
Placental villous development requires the co-ordinated action of angiogenic factors on both endothelial and trophoblast cells. Like vascular endothelial growth factor (VEGF), VEGF-C increases vascular permeability, stimulates endothelial cell proliferation and migration. In the present study, we investigated the expression of VEGF-C and its receptors VEGFR-3 and VEGFR-2 in normal and intrauterine growth-restricted (IUGR) placenta. Immunolocalisation studies showed that like VEGF and VEGFR-1, VEGF-C, VEGFR-3 and VEGFR-2 co-localised to the syncytiotrophoblast, to cells in the maternal decidua, as well as to the endothelium of the large placental blood vessels. Western blot analysis demonstrated a significant decrease in placental VEGF-C and VEGFR-3 protein expression in severe IUGR as compared to gestationally-matched third trimester pregnancies. Conditioned medium from VEGF-C producing pancreatic carcinoma (Suit-2) and endometrial epithelial (Hec-1B) cell lines caused an increased association of the phosphorylated extracellular signal regulated kinase (ERK) in VEGFR-3 immunoprecipitates from spontaneously transformed first trimester trophoblast cells. VEGF121 caused dose-dependant phosphorylation of VEGFR-2 in trophoblast cells as well as stimulating DNA synthesis. In addition, premixing VEGF165 with heparin sulphate proteoglycan potentiated trophoblast proliferation and the association of phospho-ERK with the VEGFR-2 receptor. VEGF165-mediated DNA synthesis was inhibited by anti-VEGFR-2 neutralising antibody. The results demonstrate functional VEGFR-2 and VEGFR-3 receptors on trophoblast and suggest that the decreased expression of VEGF-C and VEGFR-3 may contribute to the abnormal villous development observed in IUGR placenta.
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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/Culture Media, Conditioned,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelial Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Pregnancy Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Isoforms,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Vascular Endothelial...,
http://linkedlifedata.com/resource/pubmed/chemical/VEGFA protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor C,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0213-3911
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
16
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
359-75
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11332691-Blotting, Western,
pubmed-meshheading:11332691-Carcinoma, Pancreatic Ductal,
pubmed-meshheading:11332691-Culture Media, Conditioned,
pubmed-meshheading:11332691-Endometrium,
pubmed-meshheading:11332691-Endothelial Growth Factors,
pubmed-meshheading:11332691-Endothelium, Vascular,
pubmed-meshheading:11332691-Female,
pubmed-meshheading:11332691-Fetal Growth Retardation,
pubmed-meshheading:11332691-Humans,
pubmed-meshheading:11332691-Immunohistochemistry,
pubmed-meshheading:11332691-Infant, Newborn,
pubmed-meshheading:11332691-Lymphokines,
pubmed-meshheading:11332691-Matched-Pair Analysis,
pubmed-meshheading:11332691-Mitogen-Activated Protein Kinases,
pubmed-meshheading:11332691-Phosphorylation,
pubmed-meshheading:11332691-Placenta,
pubmed-meshheading:11332691-Pregnancy,
pubmed-meshheading:11332691-Pregnancy Proteins,
pubmed-meshheading:11332691-Protein Isoforms,
pubmed-meshheading:11332691-Receptor Protein-Tyrosine Kinases,
pubmed-meshheading:11332691-Receptors, Growth Factor,
pubmed-meshheading:11332691-Receptors, Vascular Endothelial Growth Factor,
pubmed-meshheading:11332691-Trophoblasts,
pubmed-meshheading:11332691-Tumor Cells, Cultured,
pubmed-meshheading:11332691-Vascular Endothelial Growth Factor A,
pubmed-meshheading:11332691-Vascular Endothelial Growth Factor C,
pubmed-meshheading:11332691-Vascular Endothelial Growth Factor Receptor-3,
pubmed-meshheading:11332691-Vascular Endothelial Growth Factors
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pubmed:year |
2001
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pubmed:articleTitle |
Expression of VEGF-C and activation of its receptors VEGFR-2 and VEGFR-3 in trophoblast.
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pubmed:affiliation |
Department of Reproductive and Vascular Biology, The Medical School, University of Birmingham, Edgbaston, UK.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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