File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Identification of the NF-E2-related factor-2-dependent genes conferring protection against oxidative stress in primary cortical astrocytes using oligonucleotide microarray analysis

TitleIdentification of the NF-E2-related factor-2-dependent genes conferring protection against oxidative stress in primary cortical astrocytes using oligonucleotide microarray analysis
Authors
Issue Date2003
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2003, v. 278 n. 14, p. 12029-12038 How to Cite?
AbstractThe antioxidant responsive element (ARE) mediates transcriptional regulation of phase II detoxification enzymes and antioxidant proteins such as NAD(P)H:quinone oxidoreductase (NQO1), glutathione S-transferases, and glutamate-cysteine ligase. In this study, we demonstrate that NF-E2-related factor-2 (Nrf2) plays a major role in transcriptional activation of ARE-driven genes and identify Nrf2-dependent genes by oligonucleotide microarray analysis using primary cortical astrocytes from Nrf2+/+ and Nrf2-/- mice. Nrf2-/- astrocytes had decreased basal NQO1 activity and no induction by tert-butylhydroquinone compared with Nrf2+/+ astrocytes. Similarly, both basal and induced levels of human NQO1-ARE-luciferase expression in Nrf2-/- astrocytes were significantly lower than in Nrf2+/+ astrocytes. Furthermore, human NQO1-ARE-luciferase expression in Nrf2-/- astrocytes was restored by overexpression of Nrf2, whereas ARE activation in Nrf2+/+ astrocytes was completely blocked by dominant-negative Nrf2. In addition, we observed that Nrf2-dependent genes protected primary astrocytes from H2O2-or platelet-activating factor-induced apoptosis. In support of these observations, we identified Nrf2-dependent genes encoding detoxification enzymes, glutathione-related proteins, antioxidant proteins, NADPH-producing enzymes, and anti-inflammatory genes using oligonucleotide microarrays. Proteins within these functional categories are vital to the maintenance and responsiveness of a cell defense system, suggesting that an orchestrated change in gene expression via Nrf2 and the ARE gives a synergistic protective effect against oxidative stress.
Persistent Identifierhttp://hdl.handle.net/10722/76452
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, JMen_HK
dc.contributor.authorCalkins, MJen_HK
dc.contributor.authorChan, Ken_HK
dc.contributor.authorKan, YWen_HK
dc.contributor.authorJohnson, JAen_HK
dc.date.accessioned2010-09-06T07:21:23Z-
dc.date.available2010-09-06T07:21:23Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2003, v. 278 n. 14, p. 12029-12038en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76452-
dc.description.abstractThe antioxidant responsive element (ARE) mediates transcriptional regulation of phase II detoxification enzymes and antioxidant proteins such as NAD(P)H:quinone oxidoreductase (NQO1), glutathione S-transferases, and glutamate-cysteine ligase. In this study, we demonstrate that NF-E2-related factor-2 (Nrf2) plays a major role in transcriptional activation of ARE-driven genes and identify Nrf2-dependent genes by oligonucleotide microarray analysis using primary cortical astrocytes from Nrf2+/+ and Nrf2-/- mice. Nrf2-/- astrocytes had decreased basal NQO1 activity and no induction by tert-butylhydroquinone compared with Nrf2+/+ astrocytes. Similarly, both basal and induced levels of human NQO1-ARE-luciferase expression in Nrf2-/- astrocytes were significantly lower than in Nrf2+/+ astrocytes. Furthermore, human NQO1-ARE-luciferase expression in Nrf2-/- astrocytes was restored by overexpression of Nrf2, whereas ARE activation in Nrf2+/+ astrocytes was completely blocked by dominant-negative Nrf2. In addition, we observed that Nrf2-dependent genes protected primary astrocytes from H2O2-or platelet-activating factor-induced apoptosis. In support of these observations, we identified Nrf2-dependent genes encoding detoxification enzymes, glutathione-related proteins, antioxidant proteins, NADPH-producing enzymes, and anti-inflammatory genes using oligonucleotide microarrays. Proteins within these functional categories are vital to the maintenance and responsiveness of a cell defense system, suggesting that an orchestrated change in gene expression via Nrf2 and the ARE gives a synergistic protective effect against oxidative stress.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.titleIdentification of the NF-E2-related factor-2-dependent genes conferring protection against oxidative stress in primary cortical astrocytes using oligonucleotide microarray analysisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9258&volume=278&spage=12029&epage=12038&date=2003&atitle=Identification+of+the+NF-E2-related+factor-2-dependent+genes+conferring+protection+against+oxidative+stress+in+primary+cortical+astrocytes+using+oligonucleotide+microarray+analysis.en_HK
dc.identifier.emailChan, K: kaimin@hkucc.hku.hken_HK
dc.identifier.authorityChan, K=rp00489en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1074/jbc.M211558200en_HK
dc.identifier.pmid12556532-
dc.identifier.scopuseid_2-s2.0-0038146898en_HK
dc.identifier.hkuros113816en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038146898&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume278en_HK
dc.identifier.issue14en_HK
dc.identifier.spage12029en_HK
dc.identifier.epage12038en_HK
dc.identifier.isiWOS:000182015700042-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, JM=25622544900en_HK
dc.identifier.scopusauthoridCalkins, MJ=7007180294en_HK
dc.identifier.scopusauthoridChan, K=7406032228en_HK
dc.identifier.scopusauthoridKan, YW=7102524964en_HK
dc.identifier.scopusauthoridJohnson, JA=7406813149en_HK
dc.identifier.citeulike3509448-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats