Project description:we employed DNA microarray platform to compare the gene expression patterns in primary human cardiomyocytes treated with trastuzumab (50µg/ml), trastuzumab (50µg/ml) plus pertuzumab (50µg/ml), T-DM1 (10 µg/ml), or control (no treatment).
Project description:Microarray expression data from C57/Bl6Nand b1-adrenergic transgenic mice, including heart tissue, isolated cardiomycytes and fibroblast, and lung fibroblasts Expression data was further used to identify promising targets in cardiomyocytes that are also members of the ubiquitin proteasome system that are upregulated in heart cells
Project description:This SuperSeries is composed of the following subset Series: GSE29992: Genome-wide profiling of E12.5 cardiomyocytes RNA expression in both hetozygeous control and mutant GSE29994: ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex Refer to individual Series
Project description:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. We have identified fractalkine as a possible novel mediator in HF development. To address this issue, we have performed microarray analysis of cardiomyocytes treated with different isoforms of fractalkine. Methods: Cardiomyocytes isolated from adult rat hearts and treated with different forms of fractalkine for 24 hours. Control cells were treated with BSA. Molecular alterations in myocardial tissue were measured by using cDNA microarrays. Molecular pathways affected were identified by the Ingenuity Pathway Analysis software. Results: Several molecular pathways were affected upon fractalkine stimulation of adult cardiomyocytes. Keywords: Fractalkines effect on cardiomyocytes
Project description:FGF21 belongs to the FGF superfamily and the highest expression of the FGF21 transcript was found in the liver. The initial studies identified FGF21 as an endocrine hepatokine with crucial roles in regulating lipid, glucose and energy metabolism. More recent studies have indicated a role for FGF21 in cardiovascular stress and diseases.The goal of our study is to analyze the effect of FGF21 on ischemic cardiomyocytes transcriptome using microarray. Total RNA was extracted from cultured neonatal mice cardiomyocytes after exposure to hypoxia (in 2% oxygen, 5% CO2 and 93% N2) for 12 h in the absence or presence of FGF21. Samples were processed for hybridization to the Mouse Gene 2.0 ST Array (Affymetrix). We sought to find out the differentially expressed genes regulated by FGF21 in hypoxic cardiomyocytes.
Project description:In the current study we examined several proteomic- and RNA-Seq-based datasets of cardiac-enriched, cell-surface and membrane-associated proteins in human fetal and mouse neonatal ventricular cardiomyocytes. By integrating available microarray and tissue expression profiles along with MGI phenotypic analysis, we identified 173 membrane-associated proteins that are cardiac-enriched, conserved amongst eukaryotic species, and have not yet been linked to a ‘cardiac’ Phenotype-Ontology. To highlight the utility of this dataset, we selected several proteins to investigate more carefully, including FAM162A, MCT1, and COX20, to show cardiac enrichment, subcellular distribution and expression patterns in disease. Three-dimensional imaging was used to validate subcellular localization and expression in adult mouse ventricular cardiomyocytes. FAM162A, MCT1, and COX20 were differentially expressed at the transcriptomic and proteomic levels in multiple models of mouse and human heart diseases and may represent potential diagnostic and therapeutic targets for human dilated and ischemic cardiomyopathies. Altogether, we believe this comprehensive cardiomyocyte membrane proteome dataset will prove instrumental to future investigations aimed at characterizing heart disease markers and/or therapeutic targets for heart failure.
Project description:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. We have identified fractalkine as a possible novel mediator in HF development. To address this issue, we have performed microarray analysis of cardiomyocytes treated with different isoforms of fractalkine. Methods: Cardiomyocytes isolated from adult rat hearts and treated with different forms of fractalkine for 24 hours. Control cells were treated with BSA. Molecular alterations in myocardial tissue were measured by using cDNA microarrays. Molecular pathways affected were identified by the Ingenuity Pathway Analysis software. Results: Several molecular pathways were affected upon fractalkine stimulation of adult cardiomyocytes. Experiment Overall Design: Cardiomyocytes isolated from adult rat hearts at three different timepoints. Five fractalkine treated samples and five control samples were pairwise analyzed. The cells were from three different isolations. Treated and untreated cells from the same isolation were compared on each microarray.
Project description:We generated maps of H3K4me1, H3K27ac (enhancers), H3K4me3, Pol II (promoters) and H3K27me3 (repressed chromatin) in the genome of human iPSC-derived cardiomyocytes Differentiation of cardiomyocytes from iPSC followed by ChIP-seq of H3K27ac, H34me1, H327me3, H3K4me3 and PolII