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- Publisher Website: 10.1074/jbc.M211558200
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- PMID: 12556532
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Article: Identification of the NF-E2-related factor-2-dependent genes conferring protection against oxidative stress in primary cortical astrocytes using oligonucleotide microarray analysis
Title | Identification of the NF-E2-related factor-2-dependent genes conferring protection against oxidative stress in primary cortical astrocytes using oligonucleotide microarray analysis |
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Authors | |
Issue Date | 2003 |
Publisher | American 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/76452 |
ISSN | 2020 Impact Factor: 5.157 2023 SCImago Journal Rankings: 1.766 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Lee, JM | en_HK |
dc.contributor.author | Calkins, MJ | en_HK |
dc.contributor.author | Chan, K | en_HK |
dc.contributor.author | Kan, YW | en_HK |
dc.contributor.author | Johnson, JA | en_HK |
dc.date.accessioned | 2010-09-06T07:21:23Z | - |
dc.date.available | 2010-09-06T07:21:23Z | - |
dc.date.issued | 2003 | en_HK |
dc.identifier.citation | Journal Of Biological Chemistry, 2003, v. 278 n. 14, p. 12029-12038 | en_HK |
dc.identifier.issn | 0021-9258 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/76452 | - |
dc.description.abstract | The 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.language | eng | en_HK |
dc.publisher | American Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/ | en_HK |
dc.relation.ispartof | Journal of Biological Chemistry | en_HK |
dc.rights | Journal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc. | en_HK |
dc.title | 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.type | Article | en_HK |
dc.identifier.openurl | http://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.email | Chan, K: kaimin@hkucc.hku.hk | en_HK |
dc.identifier.authority | Chan, K=rp00489 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1074/jbc.M211558200 | en_HK |
dc.identifier.pmid | 12556532 | - |
dc.identifier.scopus | eid_2-s2.0-0038146898 | en_HK |
dc.identifier.hkuros | 113816 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0038146898&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 278 | en_HK |
dc.identifier.issue | 14 | en_HK |
dc.identifier.spage | 12029 | en_HK |
dc.identifier.epage | 12038 | en_HK |
dc.identifier.isi | WOS:000182015700042 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Lee, JM=25622544900 | en_HK |
dc.identifier.scopusauthorid | Calkins, MJ=7007180294 | en_HK |
dc.identifier.scopusauthorid | Chan, K=7406032228 | en_HK |
dc.identifier.scopusauthorid | Kan, YW=7102524964 | en_HK |
dc.identifier.scopusauthorid | Johnson, JA=7406813149 | en_HK |
dc.identifier.citeulike | 3509448 | - |
dc.identifier.issnl | 0021-9258 | - |