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Titolo:
Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells
Autore:
Kim, I; Moon, SO; Kim, SH; Kim, HJ; Koh, YS; Koh, GY;
Indirizzi:
Chonbuk Natl Univ, Sch Med, Natl Creat Res Initiat Ctr Cardiac Regenerat, Chonju 560180, South Korea Chonbuk Natl Univ Chonju South Korea 560180 , Chonju 560180, South Korea Chonbuk Natl Univ, Sch Med, Dept Urol, Chonju 560180, South Korea Chonbuk Natl Univ Chonju South Korea 560180 , Chonju 560180, South Korea
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 10, volume: 276, anno: 2001,
pagine: 7614 - 7620
SICI:
0021-9258(20010309)276:10<7614:VEGFEO>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; NITRIC-OXIDE SYNTHASE; FLK-1/KDR ACTIVATION; IN-VIVO; PHOSPHORYLATION; PATHWAY; RECEPTOR; AKT; ANGIOGENESIS; CYTOKINES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Koh, GY Chonbuk Natl Univ, Sch Med, Natl Creat Res Initiat Ctr Cardiac Regenerat, San 2-20, Chonju 560180, South Korea Chonbuk Natl Univ San 2-20 Chonju South Korea 560180 South Korea
Citazione:
I. Kim et al., "Vascular endothelial growth factor expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin through nuclear factor-kappa B activation in endothelial cells", J BIOL CHEM, 276(10), 2001, pp. 7614-7620

Abstract

Vascular endothelial growth factor (VEGF) induces adhesion molecules on endothelial cells during inflammation. Here we examined the mechanisms underlying VEGF-stimulated expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1)1 and E-selectin in human umbilical vein endothelial cells. VEGF (20 ng/ml) increased expression of ICAM-1, VCAM-1, and E-selectin mRNAs in a time-dependent manner. These effects were significantly suppressed by Flk-1/kinase-insert domain containing receptor (KDR) antagonist and by inhibitors of phospholipase C, nuclear factor (NF)-B-K, sphingosine kinase, and protein kinase C, but they were not affected by inhibitors of mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) 1/2 or nitric-oxide synthase, Unexpectedly, the phosphatidylinositol (PI) 3'-kinase inhibitor wortmannin enhanced both basal and VEGF-stimulated adhesion molecule expression, whereas insulin, a PI 3'-kinase activator, suppressed both basal and VEGF-stimulated expression, Gel shift analysis revealed that VEGF stimulated NF-B-K activity, This effect was inhibited by phospholipase C, NF-B-K, or protein kinase C inhibitor, VEGFincreased VCAM-1 and ICAM-1 protein levels and increased leukocyte adhesiveness in a NF-KB-dependent manner. These results suggest that VEGF-stimulated expression of ICAM-1, VCARI-1, and E-selectin mRNAs was mainly through NF-KB activation with PI 3'-kinase-mediated suppression, but was independentof nitric oxide and MEK, Thus, VEGF simultaneously activates two signal transduction pathways that have opposite functions in the induction of adhesion molecule expression. The existence of parallel inverse signaling impliesthat the induction of adhesion molecule expression by VEGF is very finely regulated.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 19:00:34