Silencer-Mediated Repression and Non-Mediated Activation of BDNF and c-fos Gene Promoters in Primary Glial or Neuronal Cells

Tabuchi, Akiko; Nakatani, Chikako; Nakaoka, Ryuki; Naruse, Yoshihisa; Kojima, Takao; Mori, Nozomu; Tsuda, Masashi

doi:10.1006/bbrc.1999.0974

Cited by 8 publications

(3 citation statements)

References 13 publications

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“…mary glial cells but not in primary cortical neurons. 16) We wanted to identify the transcription factors that bind to NRSE/RE-1 by using the chimeric promoters of the BDNF or c-fos gene. Over-expression of the zinc finger transcription factor RE-1-silencing transcription factor (REST)/neuron-restrictive silencer factor (NRSF) 17,18) resulted in repression of BDNF promoter I activity during KCl-stimulation.…”

Section: Transcription Of the Bdnf Genementioning

confidence: 99%

Synaptic Plasticity-Regulated Gene Expression: a Key Event in the Long-Lasting Changes of Neuronal Function

Tabuchi

2008

Biological & Pharmaceutical Bulletin

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"Neuronal activity"-dependent transcriptional activation is required for the long-lasting, functional changes that are involved in memory consolidation or drug addiction. Elucidation of the molecular mechanisms underlying the neuronal activity-dependent transcription of synaptic plasticity-related genes has helped towards understanding neuronal function and disorders as well in identifying new target molecules for drug design. In this study, we focused on neurotrophin and neuropeptide, which both have the ability to modulate neuronal survival and function. We also examined the molecular mechanisms by which underlying neurotrophin genes are regulated by neuronal activity. Brain-derived neurotrophic factor (BDNF) is a neurotrophin family member that has important roles in neuronal survival and plasticity as well as in psychiatric disorders. Transcriptional activation of the BDNF gene is commonly regulated by a key transcription factor, cAMP response element-binding protein (CREB), and this at least in part contributes to neuronal activity-dependent neuronal survival. Among at least four distinct promoters of the BDNF gene, promoters I and III are differentially activated by Ca 2؉ signals via NMDA receptors and L-type voltage-dependent Ca 2؉ channels. Especially, BDNF gene promoter I activation requires the cooperative binding of and upstream stimulatory factor (USF) and CREB to a CRE/USF binding site. By contrast, NT-3 gene transcription is regulated by Sp3/4. An important future direction will be to elucidate how long-lasting changes in neuronal plasticity are "epigenetically" and "structurally" controlled. Our studies on the relationships between long-lasting neuronal responses and gene expressions should help guide research into novel drugs for neuronal or psychiatric disorders.

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Section: Transcription Of the Bdnf Genementioning

confidence: 99%

Synaptic Plasticity-Regulated Gene Expression: a Key Event in the Long-Lasting Changes of Neuronal Function

Tabuchi

2008

Biological & Pharmaceutical Bulletin

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“…Using DNA transfection in primary rat cortical neuronal cell culture, the DNA elements responsible for the Ca 2ϩ signal-mediated activation of BDNF promoter III have been identified (4,5), and furthermore, we have characterized the BDNF promoter I as a Ca 2ϩ signal-responsive promoter (13,14). In the present study, therefore, we examined whether the BDNF gene promoters I and III responded differentially or similarly to the Ca 2ϩ signals evoked via NMDA-R or L-VDCC.…”

mentioning

confidence: 97%

Differential Activation of Brain-derived Neurotrophic Factor Gene Promoters I and III by Ca2+ Signals Evoked vial-type Voltage-dependent andN-Methyl-d-aspartate Receptor Ca2+Channels

Tabuchi¹,

Nakaoka²,

Amano³

et al. 2000

Journal of Biological Chemistry

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128

111

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“…Both exons I and II of the rat BDNF gene contain a neural‐restrictive silencer element/repressor element‐1 (NSRE/RE1; Timmusk et al, 1999), to which a type of silencer protein binds to prevent the expressions of neuron‐specific genes in nonneuronal cells (Chong et al, 1995; Schoenherr and Anderson, 1995). Tabuchi et al (1999) showed that expression of an exogenous reporter gene with an NRSE/RE1 in its promoter region was repressed in primary glial cells. The expression of exon I and II BDNF mRNAs in astrocytes therefore is thought to be repressed by an NSRE/RE1‐mediated mechanism.…”

Section: Discussionmentioning

confidence: 99%

Endothelin increases expression of exon III- and exon IV-containing brain-derived neurotrophic factor transcripts in cultured astrocytes and rat brain

et al. 2005

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The effects of endothelins (ETs) on brain-derived neurotrophic factor (BDNF) production in astrocytes were investigated. ET-1 (100 nM) increased the mRNA level and extracellular release of BDNF in cultured astrocytes. RT-PCR analyses using primer pairs that amplified exon-specific BDNF transcripts revealed that exon III- and exon IV-containing BDNF transcripts existed in cultured astrocytes, whereas exon I- and exon II-containing BDNF transcripts did not. ET-1 and Ala(1,3,11,15)-ET-1, an ET(B) receptor agonist, increased the expressions of the exon III and exon IV transcripts in cultured astrocytes. Intracerebroventricular administration of 500 pmol/day of Ala(1,3,11,15)-ET-1 increased exon III and exon IV BDNF transcripts in the rat striatum. In cultured astrocytes, Ca(2+)-chelation, W-7 (a calmodulin inhibitor), and KN93 (a Ca(2+)/calmodulin kinase inhibitor) inhibited the increases in exon IV BDNF mRNA and CCAAT enhancer-binding protein beta (C/EBPbeta) levels induced by ET-1. The ET-induced increases in exon III BDNF mRNA expression and phosphorylation of cAMP response element binding protein (CREB) were reduced by Ca(2+) chelation, W-7, KN93, PD98059 (a MEK inhibitor), and wortmannin (a phosphatidylinositol 3-kinase inhibitor). These results suggest that ETs stimulate the expressions of exon III and exon IV BDNF transcripts in astrocytes through CREB and C/EBPbeta-mediated mechanisms, respectively.

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Silencer-Mediated Repression and Non-Mediated Activation of BDNF and c-fos Gene Promoters in Primary Glial or Neuronal Cells

Cited by 8 publications

References 13 publications

Synaptic Plasticity-Regulated Gene Expression: a Key Event in the Long-Lasting Changes of Neuronal Function

Synaptic Plasticity-Regulated Gene Expression: a Key Event in the Long-Lasting Changes of Neuronal Function

Differential Activation of Brain-derived Neurotrophic Factor Gene Promoters I and III by Ca2+ Signals Evoked vial-type Voltage-dependent andN-Methyl-d-aspartate Receptor Ca2+Channels

Endothelin increases expression of exon III- and exon IV-containing brain-derived neurotrophic factor transcripts in cultured astrocytes and rat brain

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