Unknown,Transcriptomics,Genomics,Proteomics

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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. 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.

ORGANISM(S): Rattus norvegicus

SUBMITTER: junjie li

PROVIDER: E-GEOD-31117 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Cardiac hypertrophy is an important and independent risk factor for the development of cardiac myopathy that may lead to heart failure. Cardiac hypertrophy manifests as an enlargement of the individual cardiomyocytes, which impairs the function of the heart. The only way to cure end-stage cardiac myopathy is by heart transplantation, a possibility limited due to lack of donor hearts. Therefore, early diagnosis of cardiac hypertrophy is needed in order to be able to initiate interventions that may prevent further progression of the disease. The mechanisms underlying the development of cardiac hypertrophy are yet not well understood. To increase the knowledge about mechanisms and regulatory pathways involved in the progression of cardiac hypertrophy, we have developed a human induced pluripotent stem cell (hiPSC)-based in vitro model of cardiac hypertrophy and performed extensive characterization of the model using multi-omics analyses. In a series of experiments, hiPSC-derived cardiomyocytes were stimulated with Endothelin-1 for 8, 24, 48 and 72 hours and their transcriptome and secreted proteome were analyzed thoroughly. The transcriptomic data show many enriched canonical pathways related to cardiac hypertrophy already at the earliest time point, e.g., cardiac hypertrophy signaling, actin cytoskeleton signaling and PI3K/AKT signaling. Cluster analysis of the differentially expressed genes showed that there are numerous clusters of genes that are dysregulated over the time period of 8 to 72h. An integrated transcriptome-secretome analysis enabled the identification of multimodal biomarkers of high relevance for monitoring early cardiac hypertrophy progression. Taken together, the results from this study demonstrate that our in vitro model displays a hypertrophic response on transcriptomic- and secreted proteomic level. The results also provide novel insight into the underlying mechanisms of cardiac hypertrophy and novel putative early cardiac hypertrophy biomarkers have been identified that will be further validated to assess their clinical relevance.

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

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