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Titolo:
Expression of VEGF-C and activation of its receptors VEGFR-2 and VEGFR-3 in trophoblast
Autore:
Dunk, C; Ahmed, A;
Indirizzi:
Univ Birmingham, Sch Med, Dept Reprod & Vasc Biol, Div Reprod & Child Hlth, Birmingham, W Midlands, England Univ Birmingham Birmingham W Midlands England ngham, W Midlands, England
Titolo Testata:
HISTOLOGY AND HISTOPATHOLOGY
fascicolo: 2, volume: 16, anno: 2001,
pagine: 359 - 375
SICI:
0213-3911(200104)16:2<359:EOVAAO>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIAL GROWTH-FACTOR; HUMAN PLACENTAL VILLI; UMBILICAL ARTERY; FETAL VASCULARIZATION; EXTRACELLULAR-MATRIX; TERMINAL VILLI; CELLS; KDR; BINDING; LOCALIZATION;
Keywords:
VEGF-C; VEGFR-2/(KDR); placenta; endothelial cells; pregnancy; IUGR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Ahmed, A Univ Birmingham, Birmingham Womens Hosp Edgbaston, Dept Reprod & Vasc Biol, Div Reprod & Child Hlth, Birmingham B15 2TG, W Midlands, EnglandUniv Birmingham Birmingham W Midlands England B15 2TG s, England
Citazione:
C. Dunk e A. Ahmed, "Expression of VEGF-C and activation of its receptors VEGFR-2 and VEGFR-3 in trophoblast", HIST HISTOP, 16(2), 2001, pp. 359-375

Abstract

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 producingpancreatic 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. VEGF(121) caused dose-dependant phosphorylation of VEGFR-2 in trophoblast cells as well as stimulating DNA synthesis. In addition, premixing VEGF(165) with heparin sulphate proteoglycan potentiated trophoblast proliferation and the association of phospho-ERK with the VEGFR-2 receptor. VEGF(165)- 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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:42:52