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Titolo:
Vascular endothelial growth factor and the in vivo increase in plasma extravasation in the hamster cheek pouch
Autore:
Feletou, M; Staczek, J; Duhault, J;
Indirizzi:
Inst Rech Servier, Dept Diabet & Malad Metab, F-92150 Suresnes, France Inst Rech Servier Suresnes France F-92150 etab, F-92150 Suresnes, France
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 6, volume: 132, anno: 2001,
pagine: 1342 - 1348
SICI:
0007-1188(200103)132:6<1342:VEGFAT>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; NITRIC-OXIDE; PERMEABILITY FACTOR; CELL GROWTH; MICROVASCULAR PERMEABILITY; FLK-1/KDR ACTIVATION; TYROSINE KINASE; FACTOR VEGF; IN-VIVO; BINDING;
Keywords:
VEGF; PlGF; VEGF receptor; nitric oxide; prostaglandins; protein kinase C; phosphatidylinositol-3-kinase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Feletou, M Inst Rech Servier, Dept Diabet & Malad Metab, 11 Rue Moulineaux, F-92150 Suresnes, France Inst Rech Servier 11 Rue Moulineaux Suresnes France F-92150 ce
Citazione:
M. Feletou et al., "Vascular endothelial growth factor and the in vivo increase in plasma extravasation in the hamster cheek pouch", BR J PHARM, 132(6), 2001, pp. 1342-1348

Abstract

1 The purpose of this study in the hamster cheek pouch was to determine whether or not vascular endothelial growth factor (VEGF) induced changes in plasma extravasation and if so, the mechanism(s) involved.2 The cheek pouch microcirculatory bed of the anaesthetized hamster was directly observed under microscope and the number of vascular leakage sites, as shown by fluorescein isothiocyanate (FITC-dextran, 150 kD) extravasation, was counted. Drugs and VEGF were applied topically. VEGF from 0.05 to 0.5mug ml(-1) (1.2 to 12 nM) produced a dose-dependent increase in the numberof microvascular leakage sites from virtually none in basal conditions to up to 250 in some pouches. The effects of VEGF (0.1 mug ml(-1) or 2.4 nM) were blocked in a concentration-dependent manner by the non-specific heparingrowth factor antagonist TBC-1635 (0.1, 1 and 3 muM). The placenta growth factor (PIGF-1: 0.1 and 0.5 mug ml-' or 3.4 and 17 nM) did not increase plasma extravasation, per se, but abolished the effects of VEGF (2.4 nM).3 The increases in microvascular leakage produced by VEGF (2.4 nM) were partially but significantly (P < 0.05) inhibited by genistein (5 and 10 <mu>M, up to 33% inhibition), LY 294002 (30 muM, 41%), bisindolylmaleimide (1 muM, 65%) and virtually abolished by indomethacin (3 muM, 88%) and L-nitro-arginine (10 muM, 95%), these drugs being inhibitors of tyrosine kinase, phosphatidylinositol-3-kinase, protein kinase C, cyclo-oxygenase and nitric oxide synthase respectively. None of these inhibitors, at the concentration tested, induced alone an increase in plasma extravasation.4 These results indicate that the VEGF-induced plasma extravasation may involve the stimulation of VEGF-R2 (Flk-1/KDR) and the activation of phosphatidylinositol-3-kinase and protein kinase C. The production of both nitric oxide and prostaglandin is required to observe an increase in vascular leakage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/04/20 alle ore 09:01:42