Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
HYPOXIA ENHANCES INDUCTION OF ENDOTHELIAL ICAM-1 - ROLE FOR METABOLIC-ACIDOSIS AND PROTEASOMES
Autore:
ZUND G; UEZON S; STAHL GL; DZUS AL; MCGOWAN FX; HICKEY PR; COLGAN SP;
Indirizzi:
BRIGHAM & WOMENS HOSP,CTR EXPT THERAPEUT & REPERFUS INJURY,DEPT ANESTHESIA,75 FRANCIS ST BOSTON MA 02115 BRIGHAM & WOMENS HOSP,CTR EXPT THERAPEUT & REPERFUS INJURY,DEPT ANESTHESIA BOSTON MA 02115 CHILDRENS HOSP,DEPT ANESTHESIA BOSTON MA 02115 HARVARD UNIV,SCH MED BOSTON MA 02115
Titolo Testata:
American journal of physiology. Cell physiology
fascicolo: 5, volume: 42, anno: 1997,
pagine: 1571 - 1580
SICI:
0363-6143(1997)42:5<1571:HEIOEI>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; INTERCELLULAR-ADHESION MOLECULE-1; BLOOD LACTATE LEVELS; E-SELECTIN; PROTEIN-DEGRADATION; SEPTIC SHOCK; CELLS; EXPRESSION; PATHWAY; ACTIVATION;
Keywords:
LEUKOCYTE; ENDOTHELIUM; INFLAMMATION; SEPSIS; INTERCELLULAR ADHESION MOLECULE 1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
G. Zund et al., "HYPOXIA ENHANCES INDUCTION OF ENDOTHELIAL ICAM-1 - ROLE FOR METABOLIC-ACIDOSIS AND PROTEASOMES", American journal of physiology. Cell physiology, 42(5), 1997, pp. 1571-1580

Abstract

Intercellular adhesion molecule 1 (ICAM-1) is an important molecule in promotion of polymorphonuclear neutrophil transendothelial migrationduring inflammation. Coincident with many inflammatory diseases is tissue hypoxia. Thus we hypothesized that combinations of hypoxia and inflammatory stimuli may differentially regulate expression of endothelial ICAM-1. Human endothelial cells were exposed to hypoxia in the presence or absence of added lipopolysaccharide (LPS) and examined for expression of functional ICAM-1. Although hypoxia alone did not induce ICAM-1, the combination of LPS and hypoxia enhanced (3 +/- 0.4-fold overnormoxia) ICAM-1 expression. Combinations of hypoxia and LPS significantly increased lymphocyte binding, and such increases were inhibited by addition of anti-ICAM-1 antibodies or antisense oligonucleotides. Hypoxic endothelia showed a >10-fold increase in sensitivity to inhibitors of proteasome activation, and combinations of hypoxia and LPS enhanced proteasome-dependent cytoplasmic-to-nuclear localization of the nuclear transcription factor-kappa B p65 (Rel A) subunit. Such proteasome activation correlated with hypoxia-evoked decreases in both extracellular and intracellular pH. We conclude from these studies that endothelial hypoxia provides a novel, proteasome-dependent stimulus for ICAM-1 induction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 02:43:01