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Expression data from Ad-atrogin-1-GFP or Ad-GFP infected cardiomyocytes

ABSTRACT: Cardiomyocyte cell death and renewal are the pivotal events in the pathogenesis of heart failure .Atrogin-1/MAFbx is an ubiquitin E3 ligase that regulates myocardial structure and function through the cellular mechanism of protein degradation. We used DNA microarrays to detail the global trends in gene expression underlying atrogin-1- overexpressed cardiomyocytes and identified distinct classes of up-regulated genes during this process. Our findings suggest that atrogin-1 plays a critical role in regulating cardiac dysfunction at transcriptional level and may provide novel insight into how atrogin-1 modulates the programming of cardiac muscle gene expression.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE31117 | GEO | 2011/08/03

SECONDARY ACCESSION(S): PRJNA144661

REPOSITORIES: GEO

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Expression data from Ad-atrogin-1-GFP or Ad-GFP infected cardiomyocytes

Project description:Cardiomyocyte cell death and renewal are the pivotal events in the pathogenesis of heart failure .Atrogin-1/MAFbx is an ubiquitin E3 ligase that regulates myocardial structure and function through the cellular mechanism of protein degradation. We used DNA microarrays to detail the global trends in gene expression underlying atrogin-1- overexpressed cardiomyocytes and identified distinct classes of up-regulated genes during this process. Our findings suggest that atrogin-1 plays a critical role in regulating cardiac dysfunction at transcriptional level and may provide novel insight into how atrogin-1 modulates the programming of cardiac muscle gene expression. Cardiomyocytes were infected with GFP control or atrogin-1 adenoviruses for RNA extraction and hybridization on Affymetrix microarrays. We sought to define the effects of atrogin-1 on the global programme of gene expression in primary cardiomyocytes. To that end, neonatal rat cardiomyocytes were infected with GFP control (G) or atrogin-1 adenovirus (A) for 24 hours.

2011-08-02 | E-GEOD-31117 | biostudies-arrayexpress

Endogenous Muscle Atrophy F-box is Involved in the Development of Cardiac Rupture After Myocardial Infarction

Project description:Muscle atrophy F-box (MAFbx/atrogin-1), an E3 ubiquitin ligase, is a crucial mediator of skeletal muscle atrophy and cardiac hypertrophy in response to pressure overload and exercise. We investigated the role of MAFbx in the regulation of cardiac remodeling following MI. A DNA microarray analysis was conducted using total RNA from wild type and MAFbx KO mouse hearts subject to permanet coronary ligation. Results provide insight into the molecular mechanism to mediate the role of MAFbx upon cardiac remodeling after myocardial infarction

2017-04-07 | GSE97494 | GEO

Expression data from Ad-β-catenin-GFP or Ad-GFP infected cardiomyocytes

2011-12-30 | GSE34772 | GEO

Expression data from Ad-β-catenin-GFP or Ad-GFP infected cardiomyocytes

Project description:The Wnt pathway is a key regulator of embryonic development, cell growth, differentiation, polarity formation, neural development, carcinogenesis, and stem cell self-renewal, and deregulation of the Wnt signalling is associated with many human disease. The central player in the Wnt pathway is β-catenin, A recent study has shown that β-catenin/Tcf/Lef signaling pathway is an essential growth-regulatory pathway in cardiomyocytes. We used DNA microarrays to detail the global trends in gene expression underlying β-catenin-overexpressed cardiomyocytes and identified distinct classes of up- or down-regulated genes during this process. Our findings suggest that β-catenin plays a critical role in regulating cardiac dysfunction at transcriptional level and may provide novel insight into how β-catenin modulates heart diseases. Cardiomyocytes were infected with GFP control or β-catenin adenoviruses for RNA extraction and hybridization on Affymetrix microarrays. We sought to define the effects of β-catenin on the global programme of gene expression in primary cardiomyocytes. To that end, neonatal rat cardiomyocytes were infected with GFP control (G) or β-catenin adenovirus (B) for 24 hours.

2011-12-30 | E-GEOD-34772 | biostudies-arrayexpress

Endogenous Muscle Atrophy F-box Regulates Pressure Overload-Induced Cardiac Hypertrophy

Project description:Muscle atrophy F-box (MAFbx) is an E3 ubiquitin ligase which plays a critical role in mediating skeletal muscle atrophy. We investigated the effect of MAFbx KO in cardiac hypertrophy in response to pressure overload. A DNA microarray analysis was conducted using total RNA prepared from wild type and MAFbx KO mouse hearts subject to transverse aortic constriction (TAC). Results provide insight into the molecular mechanism to mediate the effect of MAFbx upon pathological hypertrophy.

2011-05-01 | GSE24372 | GEO

Endogenous Muscle Atrophy F-box Regulates Pressure Overload-Induced Cardiac Hypertrophy

2011-05-01 | E-GEOD-24372 | biostudies-arrayexpress

Gene expression in mouse neonatal cardiomyocytes, cardiac fibroblasts, reprogramming failed GFP- cells, and GFP+ iCMs

Project description:The reprogramming of fibroblast cells to induced pluripotent stem (iPS) cells raises the possibility that a somatic cell could be reprogrammed to an alternative differentiated fate without first becoming a stem/progenitor cell. A large pool of fibroblast cells exists in the post-natal heart, yet no single “master regulator” of direct cardiac reprogramming has been identified. Here, we report that a combination of three developmental transcription factors (i.e., Gata4, Mef2c and Tbx5) rapidly and efficiently reprogrammed post-natal cardiac or tail-tip fibroblasts directly into differentiated cardiomyocyte-like cells. Induced cardiomyocytes expressed cardiac-specific markers, had a global gene expression profile similar to cardiomyocytes, and contracted spontaneously. Fibroblast cells transplanted into mouse hearts one day after transduction of the three factors also differentiated into cardiomyocyte-like cells. These findings demonstrate that functional cardiomyocytes can be directly reprogrammed from differentiated somatic cells by defined factors. Reprogramming of endogenous or explanted fibroblast cells might provide a source of cardiomyocytes for regenerative approaches.

2010-06-12 | GSE22292 | GEO

Direct reprogramming of mouse fibroblasts into cardiomyocytes with chemical cocktails

Project description:The direct conversion, or trans-differentiation, of non-cardiac cells into cardiomyocytes by forced expression of transcription factors and microRNAs provide promising ways of cardiac regeneration. However, genetic manipulations are still not desirable in real clinical applications. we report the generation of automatically beating cardiomyocyte-like cells from mouse fibroblasts with only chemical cocktails. These chemical-induced cardiomyocyte-like cells (CiCMs) express cardiomyocyte-specific markers, exhibit sarcomeric organization, and possess typical cardiac calcium flux and electrophysiological features. Microarray-bassed gene expression patterns of Mouse embryonic fibroblasts (MEFs), CiCMs, and cardiomyocytes(CMs) indicated a clear transition from dividing MEFs to differentiated cardiomyocyte-like state in CiCM samples. Mouse embryonic fibroblasts were treated with a small-molecule combination CRFVPT (10 μM CHIR99021 (C); 10 μM RepSox (R); 50 μM Forskolin (F); 0.5 mM VPA (V); 5 μM Parnate, (P); 1 μM TTNPB (T)) to induce transdifferentiation to chemical-induced cardiomyocyte-like cells. CiCMs beating clusters were picked at day 24 for analysis. MEFs were isolated from mouse embryos, and CMs were isolated from mouse hearts. Total RNA of MEFs, CiCMs and CMs were extracted and hybridization on Affymetrix microarrays.

2015-08-23 | E-GEOD-69924 | biostudies-arrayexpress

Gene expression in mouse embyonic cardiomyocytes, fibroblasts and adult cardiac fibroblasts

Project description:Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation. To identify candidate fibroblast-derived factors that promote myocyte proliferation, we isolated RNA from Nkx-YFP+ cardiomyocytes, embryonic cardiac fibroblasts, and adult cardiac fibroblasts and profiled mRNA expressions by microarray analyses. Arrays were performed using Affymetrix mouse Gene 1.0 ST arrays. Analysis was performed on three biological replicates of mouse embyonic cardiomyocytes, fibroblasts and adult cardiac fibroblasts.

2009-01-14 | E-GEOD-14412 | biostudies-arrayexpress

Direct reprogramming of mouse fibroblasts into cardiomyocytes with chemical cocktails

2015-08-23 | GSE69924 | GEO

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