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Titolo:
Vascular endothelial growth factor KDR receptor signaling potentiates tumor necrosis factor-induced tissue factor expression in endothelial cells
Autore:
Shen, BQ; Lee, DY; Cortopassi, KM; Damico, LA; Zioncheck, TF;
Indirizzi:
Genentech Inc, Dept Metab & Pharmacokinet, S San Francisco, CA 94080 USA Genentech Inc S San Francisco CA USA 94080 S San Francisco, CA 94080 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 7, volume: 276, anno: 2001,
pagine: 5281 - 5286
SICI:
0021-9258(20010216)276:7<5281:VEGFKR>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; PERMEABILITY FACTOR; KDR/FLK-1 RECEPTOR; FACTOR-ALPHA; TNF-ALPHA; FLK-1/KDR ACTIVATION; MITOGENIC ACTIVITY; GENE-EXPRESSION; TYROSINE KINASE; UP-REGULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Zioncheck, TF Genentech Inc, Dept Metab & Pharmacokinet, MS 70,1 DNA Way, S San Francisco, CA 94080 USA Genentech Inc MS 70,1 DNA Way S San FranciscoCA USA 94080 A
Citazione:
B.Q. Shen et al., "Vascular endothelial growth factor KDR receptor signaling potentiates tumor necrosis factor-induced tissue factor expression in endothelial cells", J BIOL CHEM, 276(7), 2001, pp. 5281-5286

Abstract

Vascular endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TNF-alpha) have been shown to synergistically increase tissue factor (TF) expression in endothelial cells; however, the role of the VEGF receptors (KDR, Flt-1, and neuropilin) in this process is unclear. Here we report that VEGF binding to the KDR receptor is necessary and sufficient for the potentiation of TNF-induced TF expression in human umbilical vein endothelial cells. TF expression was evaluated by Western blot analysis and fluorescence-activated cell sorting. In the absence of TNF-alpha, wild-type VEGF- or KDR receptor-selective variants induced an approximate 7-fold increase in totalTF expression. Treatment with TNF alone produced an approximate 110-fold increase in total TF expression, whereas coincubation of TNF-alpha with wild-type VEGF- or KDR-selective variants resulted in an approximate 250-fold increase in TF expression. VEGF lacking the heparin binding domain was also able to potentiate TF expression, indicating that heparin-sulfate proteoglycan or neuropilin binding is not required for TF up-regulation. Neither placental growth factor nor an Flt-1-selective variant was capable of inducingTF expression in the presence or absence of TNF, Inhibition of protein-tyrosine kinase or protein kinase C activity significantly blocked the TNF/VEGF potentiation of TF up-regulation, whereas phorbol 12-myristate 13-acetate, a protein kinase C activator, increased TF expression. These data demonstrate that KDR receptor signaling governs both VEGF-induced TF expression and the potentiation of TNF-induced up-regulation of TF.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 21:16:20