Induction of Cellular Antioxidative Stress Genes through Heterodimeric Transcription Factor Nrf2/Small Maf by Antirheumatic Gold(I) Compounds

Kataoka, Kohsuke; Handa, Hiroshi; Nishizawa, Makoto

doi:10.1074/jbc.m105383200

Cited by 123 publications

(73 citation statements)

References 37 publications

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“…Another putative site involves the antioxidant-responsive element. During oxidative stress, the basic leucine zipper transcription factor Nrf2 heterodimerizes with small Maf to bind and activate antioxidant-responsive element sequences (48). Although the putative regulation of Nrf2 by PI3K is poorly defined, recent reports suggest that PI3K regulates nuclear translocation of Nrf2 through actin rearrangement in response to oxidative stress (49).…”

Section: Discussionmentioning

confidence: 99%

Nerve Growth Factor Protects against 6-Hydroxydopamine-induced Oxidative Stress by Increasing Expression of Heme Oxygenase-1 in a Phosphatidylinositol 3-Kinase-dependent Manner

Salinas¹,

Díaz²,

Abraham³

et al. 2003

Journal of Biological Chemistry

233

187

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The survival signal elicited by the phosphatidylinositol 3-kinase (PI3K)/Akt1 pathway has been correlated with inactivation of pro-apoptotic proteins and attenuation of the general stress-induced increase in reactive oxygen species (ROS). However, the mechanisms by which this pathway regulates intracellular ROS levels remain largely unexplored. In this study, we demonstrate that nerve growth factor (

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Section: Discussionmentioning

confidence: 99%

Nerve Growth Factor Protects against 6-Hydroxydopamine-induced Oxidative Stress by Increasing Expression of Heme Oxygenase-1 in a Phosphatidylinositol 3-Kinase-dependent Manner

Salinas¹,

Díaz²,

Abraham³

et al. 2003

Journal of Biological Chemistry

233

187

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“…Interestingly, of the disease-modifying antirheumatic drugs (DMARDs), gold agents induce Nrf2-dependent HO-1 transcription in vitro (26). In contrast, up-regulation of HO-1 expression is found in rat adjuvant arthritis (27).…”

mentioning

confidence: 92%

Regulatory role of heme oxygenase 1 in inflammation of rheumatoid arthritis

Kobayashi

Takeno

Saito

et al. 2006

Arthritis & Rheumatism

112

103

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Objective. To examine the expression and pathogenetic roles of heme oxygenase 1 (HO-1), an inducible heme-degrading enzyme with antiinflammatory properties, in rheumatoid arthritis (RA).Methods. HO-1 expression in synovial tissue from patients with RA, patients with osteoarthritis, and patients with noninflammatory joint diseases was determined by immunoblotting and immunohistochemistry. Conclusion. Our data demonstrate that HO-1 is expressed in RA synovial tissues and plays a regulatory role in the development of inflammation. The pharmacologic effects of auranofin depend, in part, on the levels of HO-1, suggesting that HO-1 induction is a novel therapeutic strategy for RA.

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“…8). The heterodimers of the small Maf proteins and Nrf2 activate ho-1 through binding to MAREs (9)(10)(11)(12). In contrast, heterodimers of small Maf and Bach1 or Bach2 repress transcription (13)(14)(15).…”

mentioning

confidence: 99%

Heme regulates the dynamic exchange of Bach1 and NF-E2-related factors in the Maf transcription factor network

Sun

Brand

Zenke

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

319

314

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Small Maf proteins serve as dual-function transcription factors through an exchange of their heterodimerization partners. For example, as heterodimers with hematopoietic cell-specific p45 NF-E2 or NF-E2-related factors (Nrf), they activate the ␤-globin or antioxidative stress enzyme heme oxygenase 1 (HO-1) genes, respectively. In contrast, together with Bach1, they repress these same genes. However, the signals leading to this partner exchange are not known. Using chromatin immunoprecipitation assays in NIH 3T3 cells, we show that heme, an inducer of ho-1, promotes displacement of Bach1 from the MafK-occupied ho-1 enhancers, which is followed by Nrf2 binding to these elements. Whereas histone H3 at the ho-1 enhancers and promoter is hyperacetylated irrespective of gene activity, exposure of cells to heme results in de novo hyperacetylation and hypermethylation of histone H3 in the transcribed region. These data indicate that, under normal conditions, the chromatin structure of ho-1 is in a preactivation state, but transcription is repressed by Bach1. Heme induces switching of Maf dimers, resulting in ho-1 expression. Heme also promotes displacement of Bach1 from the ␤-globin locus control region without affecting MafK binding in murine erythroleukemia cells. Thus, heme functions as a signaling molecule for gene expression in higher eukaryotes.

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Induction of Cellular Antioxidative Stress Genes through Heterodimeric Transcription Factor Nrf2/Small Maf by Antirheumatic Gold(I) Compounds

Abstract: Gold(I)-

Cited by 123 publications

References 37 publications

Nerve Growth Factor Protects against 6-Hydroxydopamine-induced Oxidative Stress by Increasing Expression of Heme Oxygenase-1 in a Phosphatidylinositol 3-Kinase-dependent Manner

Nerve Growth Factor Protects against 6-Hydroxydopamine-induced Oxidative Stress by Increasing Expression of Heme Oxygenase-1 in a Phosphatidylinositol 3-Kinase-dependent Manner

Regulatory role of heme oxygenase 1 in inflammation of rheumatoid arthritis

Heme regulates the dynamic exchange of Bach1 and NF-E2-related factors in the Maf transcription factor network

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