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Article: Dexamethasone protects RAW264.7 macrophages from growth arrest and apoptosis induced by H2O2 through alteration of gene expression patterns and inhibition of nuclear factor-kappa B (NF-κB) activity

TitleDexamethasone protects RAW264.7 macrophages from growth arrest and apoptosis induced by H2O2 through alteration of gene expression patterns and inhibition of nuclear factor-kappa B (NF-κB) activity
Authors
KeywordsDexamethasone
Gene expression
Hydrogen peroxide
NF-κB activity
RAW264.7 macrophages
Issue Date2007
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicol
Citation
Toxicology, 2007, v. 236 n. 1-2, p. 16-28 How to Cite?
AbstractIn this study, the effect of dexamethasone, a synthetic glucocorticoid, on H2O2 stimulated murine RAW264.7 macrophages was investigated. It was found that dexamethasone protected the cells from apoptosis induced by H2O2. A cDNA microarray, which consists of 1000 genes selected from a mouse clone set provided from NIA, was used to study the gene expression profiles involved in the protective effect. Our data show that dexamethasone exerts the anti-apoptosis function by changing the expression patterns of many genes involved inhibiting the up-regulation of apoptosis promoting genes and the down-regulation of cell cycle stimulating genes as well as keeping the up-regulation of cell survival related genes. Our study also revealed that dexamethasone protects RAW264.7 macrophages from H2O2 induced apoptosis through blocking nuclear factor-kappa B (NF-κB) activity. © 2007 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/92805
ISSN
2015 Impact Factor: 3.817
2015 SCImago Journal Rankings: 1.335
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFong, CCen_HK
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorZhang, Qen_HK
dc.contributor.authorTzang, CHen_HK
dc.contributor.authorFong, WFen_HK
dc.contributor.authorWu, RSSen_HK
dc.contributor.authorYang, Men_HK
dc.date.accessioned2010-09-17T10:57:40Z-
dc.date.available2010-09-17T10:57:40Z-
dc.date.issued2007en_HK
dc.identifier.citationToxicology, 2007, v. 236 n. 1-2, p. 16-28en_HK
dc.identifier.issn0300-483Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/92805-
dc.description.abstractIn this study, the effect of dexamethasone, a synthetic glucocorticoid, on H2O2 stimulated murine RAW264.7 macrophages was investigated. It was found that dexamethasone protected the cells from apoptosis induced by H2O2. A cDNA microarray, which consists of 1000 genes selected from a mouse clone set provided from NIA, was used to study the gene expression profiles involved in the protective effect. Our data show that dexamethasone exerts the anti-apoptosis function by changing the expression patterns of many genes involved inhibiting the up-regulation of apoptosis promoting genes and the down-regulation of cell cycle stimulating genes as well as keeping the up-regulation of cell survival related genes. Our study also revealed that dexamethasone protects RAW264.7 macrophages from H2O2 induced apoptosis through blocking nuclear factor-kappa B (NF-κB) activity. © 2007 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicolen_HK
dc.relation.ispartofToxicologyen_HK
dc.subjectDexamethasoneen_HK
dc.subjectGene expressionen_HK
dc.subjectHydrogen peroxideen_HK
dc.subjectNF-κB activityen_HK
dc.subjectRAW264.7 macrophagesen_HK
dc.titleDexamethasone protects RAW264.7 macrophages from growth arrest and apoptosis induced by H2O2 through alteration of gene expression patterns and inhibition of nuclear factor-kappa B (NF-κB) activityen_HK
dc.typeArticleen_HK
dc.identifier.emailWu, RSS: rudolfwu@hku.hken_HK
dc.identifier.authorityWu, RSS=rp01398en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.tox.2007.03.024en_HK
dc.identifier.pmid17499901-
dc.identifier.scopuseid_2-s2.0-34248639057en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34248639057&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume236en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage16en_HK
dc.identifier.epage28en_HK
dc.identifier.isiWOS:000247355200003-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridFong, CC=11739503800en_HK
dc.identifier.scopusauthoridZhang, Y=16176894000en_HK
dc.identifier.scopusauthoridZhang, Q=35515964300en_HK
dc.identifier.scopusauthoridTzang, CH=6508203245en_HK
dc.identifier.scopusauthoridFong, WF=7102816013en_HK
dc.identifier.scopusauthoridWu, RSS=7402945079en_HK
dc.identifier.scopusauthoridYang, M=35204210300en_HK

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