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Molecular and Cellular Biology, March 2001, p. 2085-2097, Vol. 21, No. 6
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.6.2085-2097.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

The Neuron-Restrictive Silencer Element-Neuron-Restrictive Silencer Factor System Regulates Basal and Endothelin 1-Inducible Atrial Natriuretic Peptide Gene Expression in Ventricular Myocytes

Koichiro Kuwahara,1 Yoshihiko Saito,1,* Emiko Ogawa,1 Nobuki Takahashi,1 Yasuaki Nakagawa,1 Yoshihisa Naruse,2 Masaki Harada,1 Ichiro Hamanaka,1 Takehiko Izumi,1 Yoshihiro Miyamoto,1 Ichiro Kishimoto,1 Rika Kawakami,1 Michio Nakanishi,1 Nozomu Mori,2,3 and Kazuwa Nakao1

Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto 606-8397,1 Department of Molecular Genetic Research, National Institute for Longevity Sciences, Oobu, Aichi 474-8522,2 and CREST, Science and Technology Corporation of Japan (JST), Kawaguchi, Saitama 332-0012,3 Japan

Received 19 October 2000/Accepted 19 December 2000

Induction of the atrial natriuretic peptide (ANP) gene is a common feature of ventricular hypertrophy. A number of cis-acting enhancer elements for several transcriptional activators have been shown to play central roles in the regulation of ANP gene expression, but much less is known about contributions made by transcriptional repressors. The neuron-restrictive silencer element (NRSE), also known as repressor element 1, mediates repression of neuronal gene expression in nonneuronal cells. We found that NRSE, which is located in the 3' untranslated region of the ANP gene, mediated repression of ANP promoter activity in ventricular myocytes and was also involved in the endothelin 1-induced increase in ANP gene transcription. The repression was conferred by a repressor protein, neuron-restrictive silencer factor (NRSF). NRSF associated with the transcriptional corepressor mSin3 and formed a complex with histone deacetylase (HDAC) in ventricular myocytes. Trichostatin A (TSA), a specific HDAC inhibitor, relieved NRSE-mediated repression of ANP promoter activity, and chromatin immunoprecipitation assays revealed the involvement of histone deacetylation in NRSE-mediated repression of ANP gene expression. Furthermore, in myocytes infected with recombinant adenovirus expressing a dominant-negative form of NRSF, the basal level of endogenous ANP gene expression was increased and a TSA-induced increase in ANP gene expression was apparently attenuated, compared with those in myocytes infected with control adenovirus. Our findings show that an NRSE-NRSF system plays a key role in the regulation of ANP gene expression by HDAC in ventricular myocytes and provide a new insight into the role of the NRSE-NRSF system outside the nervous system.

* Corresponding author. Mailing address: Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606, Japan. Phone: 81-75-751-4287. Fax: 81-75-771-9452. E-mail: yssaito{at}kuhp.kyoto-u.ac.jp.

Molecular and Cellular Biology, March 2001, p. 2085-2097, Vol. 21, No. 6
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.6.2085-2097.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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