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:Transforming growth factor β (TGFβ) is a secreted growth factor that, in early development, is produced by cardiac myocytes and impacts fibroblasts, driving differentiation and into a differentiated state to synthesize ECM and matricellular proteins. These, in turn, impact cardiomyocyte maturation through cell-cell interactions, ECM-cellular interactions, and paracrine factors. Deletion of Tgfb1, Tgfb2, Tgfb3 genes (TGFβ ligands) from cardiomyocytes during early development in a genetically modified mouse line was found to result in cardiac dysfunction by 6 weeks of age. This indicated a definitive role for TGFβ ligands produced by cardiac myocytes in cardiac development and function. The goal of this microarray project was to transcriptionally profile hearts with cardiomyocytes that were deficient in TGFβ ligand production. In order to transcriptionally profile hearts encompassing cardiomyocytes with deficient TGFb signaling, genetically-modified mouse lines were bred in which genes encoding the TGFb ligands could be knocked out specifically in cardiomyocytes in a Cre recombinase-dependent manner. This was achieved utilizing the aMHC-Cre transgenic line where Cre-recombinase is expressed exclusively in cardiomyocytes under the aMHC promoter [PMID: 9202069]. Whole hearts were harvested from 6-week old control [aMHC-Cre transgenic] and mutant [double knockouts (DKO) with TGFb 2 and 3 deleted and triple knockouts (TKO) with TGFb 1, 2 and 3 deleted] mice. Microarray analysis was performed on total RNA isolated from biological replicates of these hearts at the Gene Expression Core Facility (CCHMC) using the Affymetrix Cariom S platform. Differential gene expression was determined by bioinformatic analysis (CEL files) using Transcriptome Analysis Console 9.
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: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:Dysregulation of miRs has been reported in a variety of cardiac diseases. In particular, it has reported that estrogen regulates a miRs network in female cardiac fibroblasts, thereby modulating a spectrum of genes involved in cardiac fibrosis and remodeling. However, the estrogen-responsive miRs in cardiomyocytes still remain to be elucidated. We used a microRNA microarray screening approach to address the miRs expression profiling in estrogen-treated cardiomyocytes.