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Global gene expression in adult cardiac fibroblasts transduced with cardiac transcription factor

ABSTRACT: Four transcription factors, GATA4, Hand2, MEF2C, Tbx5 (GHMT) activated cardiac gene expression in cardiac fibroblasts, suggesting that these factors are able to reprogram fibroblasts toward a cardaic cell fate.

ORGANISM(S): Mus musculus

PROVIDER: GSE37057 | GEO | 2012/04/06

SECONDARY ACCESSION(S): PRJNA158081

REPOSITORIES: GEO

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Global gene expression in adult cardiac fibroblasts transduced with cardiac transcription factor

Project description:Four transcription factors, GATA4, Hand2, MEF2C, Tbx5 (GHMT) activated cardiac gene expression in cardiac fibroblasts, suggesting that these factors are able to reprogram fibroblasts toward a cardaic cell fate. Total RNA isolated from adult cardiac fibroblasts transduced with empty retroviral vector or GHMT-retroviruses for 2, and 4 weeks.

2012-04-05 | E-GEOD-37057 | biostudies-arrayexpress

Dynamics of H3K4me2 during cardiac lineage reprogramming

Project description:During reprogramming of fibroblasts into cardiomyocyte-like cells by overexpression of transcription factors, GATA4, Hand2, Mef2C and Tbx5 (GHMT), H3K4Me2, an active histone code, shifts from fibroblast-exclusive peaks to cardiomyocyte-exclusive peaks. Important cardiac genes are gradually marked by this active histone marker. Mouse embryonic fibroblasts (MEFs) and neonatal mouse ventricular cardiomyocytes (NMVMs) represent fibroblasts and cardiomyocytes, respectively. Chromatins harvested from MEFs infected with retroviruses carrying GHMT at day 3, day 5, day 7 post-viral infection were prepared for immunoprecipitation.

2015-07-28 | E-GEOD-71392 | biostudies-arrayexpress

Dynamics of H3K4me2 during cardiac lineage reprogramming

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Transcriptome analysis of the effect of DAPT in GHMT-induced cardiac reprogramming

Project description:The purpose of this experiment is to anlyze the transcriptomic changes associated with Notch inhibition, by DAPT treatment, during cardiac reprogramming mediated by GHMT (Gata4, Hand2, Mef2c anf Tbx5).

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Analysis of transcriptomes during cardioac reprogramming by RNA-deep Sequencing

Project description:Fibroblasts can be reprogrammed into cardiomyocyte-like cells by overexpressing transcription factors, GATA4, Hand2, Mef2C and Tbx5 (GHMT). A83-01, an inhibitor of ALK4, ALK5 and ALK7 and two microRNA, miR-1 and miR-133 increase the efficiency of cardiac reprogramming. RNA_Seq was performed to anyalyze effects of these factors on gene expression. Total RNAs were prepared from mouse embryonic fibroblasts (MEFs); Reprogramming fibroblasts including MEFs transduced with retroviruses encoding GHMT, MEFs transduced with with retroviruses encoding GHMT plus miR-1 and miR-133 (GHMT2m), MEFs transduced with with retroviruses encoding GHMT2m treated with A83-01, at day 7 after viral transduction; and neonatal mouse cardiomyocytes (NMCMs).

2015-07-28 | E-GEOD-71405 | biostudies-arrayexpress

The histone reader PHF7 cooperates with the SWI/SNF complex at cardiac super-enhancers to promote direct cardiac reprogramming

Project description:Direct cardiac reprogramming of fibroblasts to cardiomyocytes presents an attractive therapeutic strategy to restore cardiac function following injury. Cardiac reprogramming was initially achieved through the overexpression of the transcription factors Gata4, Mef2c, and Tbx5 (GMT), and later, Hand2 (GHMT) and Akt1 (AGHMT) were found to further enhance this process. Yet, staunch epigenetic barriers severely limit the ability of these cocktails to reprogram adult fibroblasts. We undertook a screen of mammalian gene regulatory factors to discover novel regulators of cardiac reprogramming in adult fibroblasts and identified the histone reader PHF7 as the most potent activating factor. Mechanistically, PHF7 localizes to cardiac super-enhancers in fibroblasts, and through cooperation with the SWI/SNF complex, increases chromatin accessibility and transcription factor binding at these sites. Importantly, PHF7 is the first epigenetic factor found to achieve efficient reprogramming in the absence of Gata4. Here, we highlight the underexplored necessity of cardiac epigenetic modifiers, such as PHF7, in harnessing chromatin remodeling complexes to overcome critical barriers to direct cardiac reprogramming.

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Gene expression profiles of mouse embryonic fibroblasts (MEFs), induced cardiomyocytes (iCMs) and heart.

Project description:Global gene expression patterns of the iCMs shift from a MEF state toward a cardiac-like phenotype by Gata4/Mef2c/Tbx5 (GMT) or GMT/Hand2 (GHMT) transduction at 2 and 4 weeks after transduction (2W, 4W). Hand2 upregulated a panel of cardiac genes and suppressed cell cylce genes during cardiac reprogramming.

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Analysis of transcriptomes during cardioac reprogramming by RNA-deep Sequencing

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Project description:Cardiac transdifferentiation represents an attractive way of reversing heart damage caused by myocardial infarction. Yet, it is still in pre-clinical stage mainly due to the lack of efficacy with current transdifferentiation protocols. Here, we describe that dimethyl sulfoxide (DMSO) is capable of augmenting cardiomyocyte transdifferentiation in vitro. Treatment of Gata4, Hand2, Mef2c and Tbx5 (GHMT) - transduced mouse embryonic fibroblasts (MEFs) with 1% DMSO induced ~5 fold increase in the percentage of Myh6-mCherry+ cells, and significantly increased the global expression of cardiac genes. Transcriptomic studies were carried out to explore the underlying mechanism of how DMSO may enhance cardiac transdifferentiation.

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Transcriptomic analysis of ethanol, DMSO, I-CBP112 and C646 treatment on mouse embryonic fibroblasts (MEFs) during direct cardiac reprogramming

Project description:Direct cardiac reprogramming represents an attractive way of reversing heart damage caused by myocardial infarction. Yet, it is still in pre-clinical stage mainly due to the lack of efficacy with current transdifferentiation protocols. Here, we describe that dimethyl sulfoxide (DMSO) is capable of augmenting direct cardiac reprogramming in vitro. Treatment of Gata4, Hand2, Mef2c and Tbx5 (GHMT) - transduced mouse embryonic fibroblasts (MEFs) with 1% DMSO induced ~5 fold increase in the percentage of Myh6-mCherry+ cells, and significantly increased the global expression of cardiac genes. Transcriptomic studies were carried out to explore the underlying mechanism of how DMSO may enhance cardiac transdifferentiation.

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