Linked Life Data

11961404

Source:http://linkedlifedata.com/resource/pubmed/id/11961404

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-4-18
pubmed:abstractText
Leukocyte adhesion to mesothelium is an important step during peritonitis, which is mediated by adhesion molecules including vascular cell adhesion molecule-1 (VCAM-1). We investigated the effect of exogenous nitric oxide (NO) on VCAM-1 expression in cultured human peritoneal mesothelial cells and its signal transduction pathway. Mesothelial cells were exposed to tumor necrosis factor-alpha (TNF-alpha) in the presence or absence of NO donors, 3-morpholino-sydnonimine (SIN-1) and nitroprusside (NP). VCAM-1 mRNA and protein expression were measured by Northern blot analysis and flow cytometry. Nuclear factor-kappaB (NF-kappaB) binding activity was determined by electrophoretic mobility shift assay. Both SIN-1 and NP inhibited the TNF-alpha induced VCAM-1 mRNA expression in a dose dependent manner (0.25-2 mM). SIN-1 also suppressed the cell surface expression of VCAM-1 molecule. Furthermore, SIN-1 and NP inhibited the VCAM-1 mRNA expression induced by interleukin-1beta or lipopolysaccharide as well. NF-kappaB inhibitor, PDTC dose dependently inhibited the TNF-alpha induced VCAM-1 mRNA expression. SIN-1 inhibited the TNF-alpha- induced NF-kappaB binding activity. Analogue of cGMP (8-bromo-cGMP) had no significant effect on TNF-alpha-induced VCAM-1 mRNA expression and guanylate cyclase inhibitor (ODQ) also had no significant influence on the inhibitory effect of SIN-1. These results suggest that exogenous NO inhibits VCAM-1 expression via suppression of NF-kappaB through a cGMP-independent pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/3-morpholino-sydnonimine, http://linkedlifedata.com/resource/pubmed/chemical/8-bromocyclic GMP, http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP, http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1, http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides, http://linkedlifedata.com/resource/pubmed/chemical/Molsidomine, http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Donors, http://linkedlifedata.com/resource/pubmed/chemical/Nitroprusside, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha, http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0028-2766
pubmed:author
pubmed:copyrightInfo
Copyright 2002 S. Karger AG, Basel
pubmed:issnType
Print
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
447-54
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Exogenous nitric oxide inhibits VCAM-1 expression in human peritoneal mesothelial cells. Role of cyclic GMP and NF-kappaB.
pubmed:affiliation
Department of Internal Medicine, College of Medicine, University of Ulsan, Seoul, Korea. sklee2@www.amc.seoul.kr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't