Project description:Differentiation and maintenance of cardiac muscle is a complex biological process. MEF2D appears to play an important role in the regulation of cardiomyocyte homeostasis. We knocked down expression of MEF2D in NRVMs, and assessed global expression pattern changes in MEF2D knockdown against a negative control. NRVMs were extracted from 1 to 2 day old rat pups and were allowed to recover for 24 hours before being transduced with shRNA viral vectors to knockdown expression of MEF2D or LacZ (negative control). After 3 days, total RNA was harvested for Affymetrix global gene expression microarray analysis. Each array was pooled RNA from six biological replicates.
Project description:Neonatal rat ventricle myocytes (NRVMs) were infected with CryABR120G adenovirus. Knockdown or overexpression of Ube2v1 was performed by siUbe2v1 transfection or AdUbe2v1 infection in CryABR120G-expressing cells. Total RNA was extracted from NRVMs of four groups: CTR (untreated control), R120G (AdCryABR120G infection), RSIV1 (AdCryABR120G infection with siUbe2v1 transfection), and RADV1 (coinfection with AdCryABR120G and AdUbe2v1), in triplicate, for gene expression profiling.
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:Differentiation and maintenance of cardiac muscle is a complex biological process. MEF2D appears to play an important role in the regulation of cardiomyocyte homeostasis. We knocked down expression of MEF2D in NRVMs, and assessed global expression pattern changes in MEF2D knockdown against a negative control.
Project description:Heart failure is a leading cause of death in US. Hypertension is one of the most important risk factor of heart failure. In the presence of high blood pressure, the heart manifests hypertrophic growth to ameliorate ventricular wall stress. This once adaptive response may progress into decompensation and heart failure. The precise mechanisms governing this transition remain elusive. Here, we aimed to identify novel signaling pathways in cardiac hypertrophic growth. Primary neonatal rat ventricular myocytes (NRVMs) were isolated from 1-2 days old rats and treated with phenylephrine or IGF-1. Total RNA was isolated for RNA-seq analysis.
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.
