Linked Life Data

12112002

Source:http://linkedlifedata.com/resource/pubmed/id/12112002

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-7-11
pubmed:abstractText
Induction of heme oxygenase (HO)-1 during inflammation has been demonstrated in many cell types, but the contribution of inflammatory molecules nitric oxide (NO) and prostaglandin E(2) (PGE(2)) has remained unresolved. Here we show that NO donors including sodium nitroprusside (SNP) and spermine nonoate (SP-NO), and PGE(2) significantly stimulate HO-1 expression in RAW264.7 macrophages, associated with alternative induction on NO and PGE(2) in medium, respectively. NO donors also show the inductive effect on cyclo-oxygenase 2 protein and PGE(2) production. In the presence of lipopolysaccharide and interferon-gamma (LPS/IFN-gamma), HO-1 protein was induced slightly but significantly, and SNP, SP-NO, and PGE(2) enhanced HO-1 protein induced by LPS/IFN-gamma. L-Arginine analogs N-nitro-L-arginine methyl ester (L-NAME) and N-nitro-L-arginine (NLA) significantly block HO-1 protein induced by LPS/IFN-gamma associated with a decrease in NO (not PGE(2)) production. And, NSAIDs aspirin and diclofenase dose dependently inhibited LPS/IFN-gamma-induced HO-1 protein accompanied by suppression of PGE(2) (not NO) production. PD98059 (a specific inhibitor of MEKK), but not SB203580 (a specific inhibitor of p38 kinase), attenuated PGE(2) (not SP-NO) induced HO-1 protein. Under UVC (100 J/m(2)) and UVB (50 J/m(2)) irradiation, PGE(2) or SP-NO treatment prevents cells from UVC or UVB-induced cell death, and HO-1 inhibitor tin protoporphyrin (SnPP) reverses the preventive effects of PGE(2) and SP-NO. The protective activity induced by PGE(2) on UVC or UVB irradiation-induced cell death was blocked by MAPK inhibitor PD98059 (not SB203580). These results demonstrated that inflammatory molecules NO and PGE(2) were potent inducers of HO-1 gene, and protected cells from UV-irradiation-induced cell death through HO-1 induction.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0730-2312
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
331-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12112002-Animals, pubmed-meshheading:12112002-Cell Death, pubmed-meshheading:12112002-Cell Line, pubmed-meshheading:12112002-Cell Survival, pubmed-meshheading:12112002-Dinoprostone, pubmed-meshheading:12112002-Drug Synergism, pubmed-meshheading:12112002-Enzyme Induction, pubmed-meshheading:12112002-Heme Oxygenase (Decyclizing), pubmed-meshheading:12112002-Heme Oxygenase-1, pubmed-meshheading:12112002-Interferon-gamma, pubmed-meshheading:12112002-Lipopolysaccharides, pubmed-meshheading:12112002-Macrophages, pubmed-meshheading:12112002-Membrane Proteins, pubmed-meshheading:12112002-Mice, pubmed-meshheading:12112002-Mitogen-Activated Protein Kinases, pubmed-meshheading:12112002-Nitric Oxide, pubmed-meshheading:12112002-Nitric Oxide Donors, pubmed-meshheading:12112002-Ultraviolet Rays
pubmed:year
2002
pubmed:articleTitle
Nitric oxide and prostaglandin E2 participate in lipopolysaccharide/interferon-gamma-induced heme oxygenase 1 and prevent RAW264.7 macrophages from UV-irradiation-induced cell death.
pubmed:affiliation
Graduate Institute of Pharmacognosy Science, Taipei Medical University, Taiwan. yc3270@tmu.edu.tw
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't