FOG-2 Competes with GATA-4 for Transcriptional Coactivator p300 and Represses Hypertrophic Responses in Cardiac Myocytes

Hirai, Masana; Ono, Koh; Morimoto, Tatsuya; Kawamura, Teruhisa; Wada, Hiromichi; Kita, Toru; Hasegawa, Koji

doi:10.1074/jbc.m401737200

Cited by 34 publications

(33 citation statements)

References 37 publications

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“…These factors interact with GATA4 and enhance gene transcription. [48][49][50] Friend of GATA (FOG)-2 is a transcriptional co-factor, and its interaction with GATA4 competes with the interaction of GATA4 with p300 and results in the repression of target genes in cardiac myocytes 51) . GATA6 is a member of the GATA family and is expressed in cardiomyocytes.…”

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confidence: 99%

Regulation of Cardiac Transcription Factor GATA4 by Post-Translational Modification in Cardiomyocyte Hypertrophy and Heart Failure

et al. 2016

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SummaryHeart failure is a leading cause of cardiovascular mortality in industrialized countries. During development and deterioration of heart failure, cardiomyocytes undergo maladaptive hypertrophy, and changes in the cellular phenotype are accompanied by reinduction of the fetal gene program. Gene expression in cardiomyocytes is regulated by various nuclear transcription factors, co-activators, and co-repressors. The zinc finger protein GATA4 is one such transcription factor involved in the regulation of cardiomyocyte hypertrophy. In response to hypertrophic stimuli such as those involving the sympathetic nervous and renin-angiotensin systems, changes in protein interaction and/or post-translational modifications of GATA4 cause hypertrophic gene transcription in cardiomyocytes. In this article, we focus on cardiac nuclear signaling molecules, especially GATA4, that are promising as potential targets for heart failure therapy. (Int Heart J 2016; 57: 672-675)

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confidence: 99%

Regulation of Cardiac Transcription Factor GATA4 by Post-Translational Modification in Cardiomyocyte Hypertrophy and Heart Failure

et al. 2016

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“…27 A total of 50 myocardial fibers were selected randomly from myocytes stained with anti-β-MHC antibody, which reacts with both α-and cardiac β-MHC. The surface area of the cells was measured semi-automatically with the aid of an image analyzer (Image Pro-Plus), as described previously.…”

Section: Immunocytochemistry and Measurement Of Cell Surface Areamentioning

confidence: 99%

“…The surface area of the cells was measured semi-automatically with the aid of an image analyzer (Image Pro-Plus), as described previously. 27 RT-PCR Total RNA from cardiomyocytes was isolated, reverse-transcribed, and amplified as described previously. 28 Primer sequences and PCR conditions of CYP11B2 and GAPDH were as described previously.…”

Section: Immunocytochemistry and Measurement Of Cell Surface Areamentioning

confidence: 99%

Aldosterone Signaling Associates With p300/GATA4 Transcriptional Pathway During the Hypertrophic Response of Cardiomyocytes

Yoshida

Morimoto

Takaya

et al. 2010

Circ J

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Background: Aldosterone exerts its effect by binding to specific mineralocorticoid receptors (MRs). Spironolactone blocks the aldosterone system, which ameliorates heart failure in humans, but the precise molecular mechanisms of MR blockade are unclear. Methods and Results:Neonatal rat cardiomyocytes were stimulated with phenylephrine (PE), aldosterone, and/or spironolactone. The association of the MR with p300, a transcriptional coactivator of GATA4 required for hypertrophic responses, was examined. MR and p300 synergistically activated GATA4-dependent atrial natriuretic factor (ANF) promoter activities. The stimulation of cardiomyocytes with PE induced translocation of the MRs into the nuclei and markedly increased the association of MRs with p300. Compatible with the synergistic activation by the MR and p300, aldosterone further augmented the PE-induced increase in cell size and induction of ANF gene transcription. Blockade of MR activation by spironolactone inhibited the PE-induced nuclear translocation of MRs and hypertrophic responses. Conclusions:For the first time it has been demonstrated that the aldosterone/MR system associates with the p300/GATA4 transcriptional pathway during the hypertrophic response of cardiomyocytes, and may provide a mechanism of the beneficial effects of aldosterone-blocking agents in heart failure therapy in humans. (Circ J 2010; 74: 156 - 162)

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“…30,31) Moreover, calcineurin-nFAT or Rho-RocK signals are also involved in GATA4 activation, 32,33) and friend of GATA (FoG)-2 functions as a repressor of the activation. 34) Acetylation of not only the histone tail but also some transcription factors is a critical process in the activation of gene transcription. We show that p300 binds and acetylates GATA4, and the acetylation enhances GATA4-induced hypertrophic gene transcriptions.…”

Section: Pathophysiological and Pharmacological Research In Cardiologymentioning

confidence: 99%

Application of Curcumin to Heart Failure Therapy by Targeting Transcriptional Pathway in Cardiomyocytes

Sunagawa

Hasegawa

Morimoto

2013

Biological & Pharmaceutical Bulletin

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Heart failure is one of the leading causes of death throughout the world. During the development and deterioration processes of heart failure, cardiomyocytes undergo maladaptive hypertrophy by altering hypertrophy-related gene expression. The zinc finger protein GATA4 is one of the transcription factors involved in the regulation of cardiomyocyte hypertrophy. In response to hypertrophic stimuli such as the synaptic nervous and rennin-angiotensin systems, GATA4 forms a large complex with various functional proteins including an intrinsic histone acetyltransferase, p300, and the disruption of this complex results in the inhibition of hypertrophic responses in cardiomyocytes. While such a transcriptional signal pathway is recognized as a critical event during cardiomyocyte hypertrophy, pharmacological heart failure therapy that targets this pathway has not been established. In order to develop novel heart failure therapy targeting the pathway in cardiomyocytes, we have studied the potential of curcumin, a p300 histone acetyltransferase inhibitor, as an agent for novel heart failure therapy. In this review, we describe a recent study on the cardiac transcriptional signal pathway, especially p300/GATA4 pathway, and a novel heart failure therapy using curcumin.

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FOG-2 Competes with GATA-4 for Transcriptional Coactivator p300 and Represses Hypertrophic Responses in Cardiac Myocytes

Cited by 34 publications

References 37 publications

Regulation of Cardiac Transcription Factor GATA4 by Post-Translational Modification in Cardiomyocyte Hypertrophy and Heart Failure

Regulation of Cardiac Transcription Factor GATA4 by Post-Translational Modification in Cardiomyocyte Hypertrophy and Heart Failure

Aldosterone Signaling Associates With p300/GATA4 Transcriptional Pathway During the Hypertrophic Response of Cardiomyocytes

Application of Curcumin to Heart Failure Therapy by Targeting Transcriptional Pathway in Cardiomyocytes

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