Project description:We compared the transcriptome modified by siRNA-mediated cardiac hypertrophy associated epigenentic regulator (Chaer) with negative control siRNA treated neonatal rat ventricular myocytes with or without phenylephrine treatment. The results suggest that Chaer knockdown broadly blocks the phenylephrine-induced hypertrophic programming of the transcriptome. Transcripts profiles from neonatal rat ventricular myocytes with or without phenylephrine and with or without Chaer-specific siRNA compared to negative control siRNA
Project description:To identify N6-methyladenosine RNA methylome in cyclophosphamide-treated neonatal rat cardiac myocytes (NRCMs), MeRIP-seq of NRCMs treated with cyclophosphamide (CYP) or solvent control (DMSO) were performed.
Project description:Title: Changes in gene expression affected by H2O2 in cardiac myocytes.<br/> Description: We aim to identify the changes in gene expression in response to <br/> oxidative stress in rat neonatal ventricular myocytes.<br/> Oxidative stress will be induced by dosing neonatal ventricular myocyte<br/> cultures with 0.2, 0.1 and 0.04mM hydrogen peroxide at 2, 4 and 8 hr time<br/> points using unstimulated myocytes as control.
Project description:We compared the transcriptome modified by siRNA-mediated cardiac hypertrophy associated epigenentic regulator (Chaer) with negative control siRNA treated neonatal rat ventricular myocytes with or without phenylephrine treatment. The results suggest that Chaer knockdown broadly blocks the phenylephrine-induced hypertrophic programming of the transcriptome.
Project description:Loss of KChIP2 during cardiac stress has been suggested to have a transcriptional impact on cardiac ion channels through altered miRNA activity, contributing to maladaptive electrical remodeling. Therefore, we tested the consequence of KChIP2 loss, in the absence of cardiac stress, by treating cultured neonatal rat ventricular myocytes with siRNA for KChIP2 and subsequently performed miRNA microarray analysis to identify up-regulation of potential miRNA targets.
Project description:Title: Regulation of gene expression through mitogen-activated protein kinase cascades in cardiac myocytes.<br/> Description: The aim of this study is to identify the changes in gene expression induced in rat neonatal <br/> ventricular myocytes, a well-established cell culture model, by endothelin-1, <br/> a known hypertrophic agonist, and to determine which of the changes are <br/> mediated through the ERK cascade. This continues TKAC^Ys previous study of the <br/> effects of oxidative stress, which induces cardiac myocyte apoptosis.<br/>