Linked Life Data

8810635

Source:http://linkedlifedata.com/resource/pubmed/id/8810635

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1996-11-4
pubmed:abstractText
To investigate the mechanisms regulating hyperoxia-induced intercellular adhesion molecule-1 (ICAM-1) expression, we studied the effects of antioxidants on ICAM-1 expression, and the relationship between ICAM-1 expression and extracellular glutathione levels in human pulmonary artery endothelial cells (HPAEC) and human umbilical vein endothelial cells (HUVEC). Cells were cultured to confluence and exposed to hyperoxia (90% O2) for 48 h with or without various antioxidants, including superoxide dismutase (SOD), catalase, N-acetylcysteine (NAC), and glutathione. The levels of ICAM-1 expression in the endothelial cells and the concentrations of reduced (GSH) and oxidized glutathione (GSSG) in the media were examined by flow cytometry and spectrophotometry, respectively. After exposure to hyperoxia, ICAM-1 expression was increased, and the supernatant total glutathione was decreased as compared with those at normoxia. SOD did not change ICAM-1 expression. The hyperoxia-induced increase in ICAM-1 expression was even greater with the addition of catalase. The ICAM-1 expression was decreased and the GSH concentration was increased with the addition of NAC. There were negative relationships between the level of ICAM-1 expression and the supernatant total glutathione concentration in catalase-treated HPAEC (R = 0.822, P < 0.0005) and HUVEC (R = 0.567, P < 0.01). Negative relationships were also demonstrated between the level of ICAM-1 expression and the total extracellular glutathione concentrations in NAC-treated HPAEC (R = 0.877, P < 0.0005) and HUVEC (R = 0.727, P < 0.0005). Exogenous GSH decreased ICAM-1 expression in both hyperoxia-exposed HPAEC and HUVEC, while exogenous GSSG did not. These results suggest that extracellular GSH plays a role in regulating hyperoxia-induced ICAM-1 expression in HPAEC and HUVEC.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
319-27
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Modulation of ICAM-1 expression by extracellular glutathione in hyperoxia-exposed human pulmonary artery endothelial cells.
pubmed:affiliation
Department of Medicine, School of Medicine, Keio University, Tokyo, Japan.
pubmed:publicationType
Journal Article