Project description:High-resolution chromosome conformation capture-sequencing of wildtype mice left ventricle after cardiac stress (i.e. hypertrophy and myocardial infarction)
Project description:We employed the Affymetrix GeneChip technology to evaluate the patterns of expression in two different in vivo models of cardiac remodeling and in two different regions (left ventricle free wall and septum) of the heart. Mice underwent transverse aortic constriction (TAC); myocardial infarction (MI) or Sham operation and RNA from the left ventricle free wall and the septum was isolated 1 week later.
Project description:To investigate the transcriotome alteration in endothelial cells (ECs) under a myocardial infarction (MI) condition, we performed RNA sequcening analysis with sorted ECs derived from mouse infarcted cardiac tissues or normal left ventricle (LV).
Project description:We employed the Affymetrix GeneChip technology to evaluate the patterns of expression in two different in vivo models of cardiac remodeling and in two different regions (left ventricle free wall and septum) of the heart. Mice underwent transverse aortic constriction (TAC); myocardial infarction (MI) or Sham operation and RNA from the left ventricle free wall and the septum was isolated 1 week later. Keywords: other
Project description:Macrophage secretome- Macrophages were isolated from the left ventricle from control (day 0) or from the infarct region at day 1 after myocardial infarction (MI). Cells were isolated in RPMI media with 0.1% fetal bovine serum and incubated for 2 hours and then spun at 800g for 5 min to separate cell debris. The sample sizes are n=4 biological replicates for each time point.
Project description:To investigate the transcriotome alteration in myocardial infarction (MI)-associated cells, we performed RNA sequcening analysis with single cells derived from mouse infarcted cardiac tissues or normal left ventricle (LV). Particularly, cardiac endothelial cells (ECs) were traced using a Cdh5-Cre;LSL-tdTomatom system.
Project description:Objectives Transcriptome analysis of the left ventricle (LV) aimed to identify targets for prevention of myocardial fibrosis (MF). Background MF causing heart failure with reduced ejection fraction is generated by different pathological mechanisms. We have designed two types of MF by using translational animal models: reactive interstitial MF and replacement fibrosis. Methods Domestic pigs were treated with either doxorubicin (DOX, n=5) or a liposomal encapsulation of doxorubicin-citrate (Myocet®, MYO, n=5) to generate cardiotoxicity-induced MF. For pressure overload-induced MF, we used artificial isthmus stenosis with stepwise developing myocardial hypertrophy and final fibrosis (Hyper, n=3). Volume-overload MF was developed in adverse remodeled LV after myocardial infarction (RemoLV, n=3). Sham interventions served as controls (Control, n=3). Myocardial samples from the anterior wall of groups DOX, MYO, Hyper and Control, and from the non-ischemic remodeled posterior wall of animals in group RemoLV were subjected to RNA-sequencing following transcriptional analysis.
Project description:To analyze early transcriptional events in cardiac tissue after infarction and evaluate the genetic expression profile of post-infarction mesenchymal cells of the heart, we induced myocardial infarction in rats by ligation of the left coronary artery. 24 hours after surgery, the affected area was harvested for RNA isolation and cell culture. We then performed a gene expression profile analysis using data obtained from RNA sequencing of 3 different postinfarction tissues and cells. Healthy tissues and cells of the left ventricle of the heart of sham-operated rats were used as controls.
