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Nucleic Acids Research Advance Access published online on October 28, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp865
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© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin and Epigenetics

Expression of stress-response ATF3 is mediated by Nrf2 in astrocytes

Kyu-Han Kim1, Jae-Yeon Jeong1, Young-Joon Surh2 and Kyu-Won Kim3,*

1NeuroVascular Coordination Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, 2National Research Laboratory of Molecular Carcinogenesis and Chemoprevention, College of Pharmacy and 3NeuroVascular Coordination Research Center, College of Pharmacy and Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 151-742, Korea

*To whom correspondence should be addressed. Tel: +82 2 880 6988; Fax: +82 2 885 1827; Email: qwonkim{at}plaza.snu.ac.kr

Received June 14, 2009. Revised September 7, 2009. Accepted September 29, 2009.

Activating Transcription Factor 3 (ATF3), a member of the ATF/CREB family, is induced rapidly by various stresses. Its induction mechanism and role in response to changes in cellular redox status, however, have not been elucidated. Here, we found that NF-E2-related factor 2 (Nrf2), a transcription factor known to bind to antioxidant response element (ARE) in promoters, transcriptionally upregulated ATF3 expression in astrocytes. Treatment with Nrf2 activators and oxidants provoked ATF3 induction in astrocytes, whereas its expression was reduced in Nrf2-depleted cells. We further demonstrated that the consensus ARE in the ATF3 promoter is critical for Nrf2-mediation by promoter analyses using an ATF3 promoter-driven luciferase construct and a chromatin immunoprecipitation assay. In addition, we found that Nrf2-dependent ATF3 induction contributed to the antioxidative and cytoprotective functions of Nrf2 in astrocytes. Taken together, our findings suggest that ATF3 is a new target for Nrf2 and has a cytoprotective function in astrocytes.


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