ArticleJournal of molecular and cellular cardiology2015
MITF interacts with the SWI/SNF subunit, BRG1, to promote GATA4 expression in cardiac hypertrophy.
Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- Genomic analyses implicate noncoding de novo variants in congenital heart disease.Nature genetics · 2020Trial
- BRG1 exacerbates myocardial fibrosis after myocardial infarction by interacting with ZEB1.Frontiers in pharmacology · 2026Article
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- Cardiac-specific deletion of BRG1 ameliorates ventricular arrhythmia in mice with myocardial infarction.Acta pharmacologica Sinica · 2024Article
- Genetic Determinants of the Interventricular Septum Are Linked to Ventricular Septal Defects and Hypertrophic Cardiomyopathy.Circulation. Genomic and precision medicine · 2023Article
- Single-nucleus transcriptomics reveals a gatekeeper role for FOXP1 in primate cardiac aging.Protein & cell · 2023Article
- Superfamily II helicases: the potential therapeutic target for cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Genetic and phenotypic profiling of supranormal ejection fraction reveals decreased survival and underdiagnosed heart failure.European journal of heart failure · 2022Article
- The role and molecular mechanism of epigenetics in cardiac hypertrophy.Heart failure reviews · 2021Review
- The role of DNA methylation in syndromic and non-syndromic congenital heart disease.Clinical epigenetics · 2021Review
- SOX4 and SMARCA4 cooperatively regulate PI3k signaling through transcriptional activation of TGFBR2.NPJ breast cancer · 2021Article
- Arteriovenous Fistula-induced Cardiac Remodeling Shows Cardioprotective Features in Mice.JVS-vascular science · 2021Article
- Substance P Administered after Myocardial Infarction Upregulates Microphthalmia-Associated Transcription Factor, GATA4, and the Expansion of c-KitStem cells international · 2020Article
- The Role of BRG1 in Antioxidant and Redox Signaling.Oxidative medicine and cellular longevity · 2020Review
- Kindlin-2 suppresses transcription factor GATA4 through interaction with SUV39H1 to attenuate hypertrophy.Cell death & disease · 2019Article
- Epigenetics in dilated cardiomyopathy.Current opinion in cardiology · 2019Review
- Vitiligo and melanocytic nevi: New findings in Coffin-Siris syndrome associated withJAAD case reports · 2019Article
- SETD7 in cardiomyocyte differentiation and cardiac function.Stem cell investigation · 2019Article
- Epigenetics of metabolic syndrome.Physiological genomics · 2018Review
- Co-sequencing and novel delayed anti-correlation identify function for pancreatic enriched microRNA biomarkers in a rat model of acute pancreatic injury.BMC genomics · 2018Article
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8 authors at 1 institution in 1 country.
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Abstract
The transcriptional regulation of pathological cardiac hypertrophy involves the interplay of transcription factors and chromatin remodeling enzymes. The Microphthalmia-Associated Transcription Factor (MITF) is highly expressed in cardiomyocytes and is required for cardiac hypertrophy. However, the transcriptional mechanisms by which MITF promotes cardiac hypertrophy have not been elucidated. In this study, we tested the hypothesis that MITF promotes cardiac hypertrophy by activating transcription of pro-hypertrophy genes through interactions with the SWI/SNF chromatin remodeling complex. In an in vivo model of cardiac hypertrophy, expression of MITF and the BRG1 subunit of the SWI/SNF complex increased coordinately in response to pressure overload. Expression of MITF and BRG1 also increased in vitro when cardiomyocytes were stimulated with angiotensin II or a β-adrenergic agonist. Both MITF and BRG1 were required to increase cardiomyocyte size and activate expression of hypertrophy markers in response to β-adrenergic stimulation. We detected physical interactions between MITF and BRG1 in cardiomyocytes and found that they cooperate to regulate expression of a pro-hypertrophic transcription factor, GATA4. Our data show that MITF binds to the E box element in the GATA4 promoter and facilitates recruitment of BRG1. This is associated with enhanced expression of the GATA4 gene as evidenced by increased Histone3 lysine4 tri-methylation (H3K4me3) on the GATA4 promoter. Thus, in hypertrophic cardiomyoctes, MITF is a key transcriptional activator of a pro-hypertrophic gene, GATA4, and this regulation is dependent upon the BRG1 component of the SWI/SNF complex.
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