Project description:The objective of this study was to investigate changes in rat cardiac ventricle transcriptome with age. It was run along similar with other tissues to look for common ageing signatures. Particular interest would be cardiomyocytes, but this is bulk RNA-sequencing.
Project description:Study of the effect of interleukin 33 (IL33) on transcript expression in neonatal rat ventricular cardiac myocytes at 0.5, 1 or 2 h
Project description:The aim of this study was to compare the most common immortalized cardiac cell lines (human: AC16, rat: H9C2, mouse: HL-1) to primary cultures (neonatal rat or mouse cardiomyocytes, and human induced pluripotent stem cells) and left ventricular tissues from the corresponding species. To characterize cardiac cell lines, cardiac cell lines were seeded onto plates, and their differentiation towards a more cardiac phenotype was induced on the basis of most commonly used protocols in literature. The cells were harvested either in stage of proliferation or differentiation, and left ventricular tissue from each corresponding species, and isolated neonatal primary cardiac myocytes (for mouse and rat) or human induced pluripotent stem cells were applied as references for comparison. Transcriptomic analysis was performed on all samples. Generally, the mRNA expression pattern of cardiac markers in the cell lines showed significant differences compared to corresponding tissue or primary cultures. mRNA profile of cell lines indicates poor cardiac characteristics regardless the differentiation protocol used. Limitations of these cell lines should be taken into account when these cells are used as in vitro platforms to model cardiomyocytes and cardiovascular diseases.
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/>
Project description:Loss of KChIP2 during cardiac stress has been suggested to have a transcriptional impact on cardiac ion channels 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 shRNA for KChIP2 and subsequently performed whole-transcriptome microarray analysis to identify gene changes.
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: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