Project description:Differential gene expressions were constructed through expression profiling of a total of 26,423 genes in the hypertrophic heart followed by pressure-overload model, then 537 significant differential genes were filtered based on the criteria (p<0.05 and fold change >1.5).
Project description:Background: Current mammalian model for heart regeneration research is limited in apex amputation or myocardium infarction, both of which are controversy. Moreover, RNAseq demonstrated there were a very limited set of differential expressed genes between sham and operation heart in the myocardium infarction model. Here we investigated whether pressure overload in the right ventricle(RV), a common phenomenon in congenital heart disease children, could be a better animal model for heart regeneration study when consider cardiomyocyte(CM) proliferation as the most important index. Methods and results: Pressure overload was induced by pulmonary artery banding (PAB) on day1 and confirmed by echocardiography and hemodynamic measurements at postnatal day 7(P7). RNAseq analyses of purified RVCM at P7 from PAB and sham-operated rats revealed there were 5469 differential expressed genes between these two groups. GO and KEGG analysis showed that these genes mainly mediated mitosis and cell division. Cell proliferation assay indicates a continuous over-proliferation of RVCM after PAB, in particular for P3. In addition, there were ~2 times-fold increase of Ki67/Phh3 -positive CM in human overload RV compared to non-overload RV. Other features about this model included CM hypotrophy and no fibrosis.. Conclusions: Pressure overload profoundly promotes RVCM proliferation in the neonatal stage both in rats and human beings, activated a regeneration-specific gene program, and may offer a better alternative animal model for heart regeneration research..
Project description:We used spontaneously hypertensive rats (SHRs) as an animal model of hypertensive heart disease and treated them with allisartan orally. We continuously monitored the rats' blood pressure levels, measured their body and heart weights, and evaluated their cardiac structure and function using echocardiography. We performed proteome analysis using the tandem mass tag (TMT) technology.
Project description:The endogenous peptide Apelin is crucial for maintaining heart function in pressure overload and aging Experiment Overall Design: Heart samples from Apelin knockout mice with pressure overload and sham control together with the wild-type mice with pressure overload and sham were compared
Project description:Differential regulation of extracellular matrix constituents in myocardial remodeling with and without heart failure following pressure overload
Project description:The expression of the small molecular weight heat shock protein (Hsp) H11 kinase/Hsp22 (Hsp22) is restricted to a limited number of tissues, including the heart and skeletal muscle, both in rodents and in humans. We generated a mouse knockout (KO) model, and investigated the role of Hsp22 in regulating cardiac hypertrophy in response to pressure overload. We compared gene expression profiles between WT and KO mice in basal condition and three days pressure overload after transverse aortic constriction (TAC). These data illustrated a novel mechanism of Hsp22-related gene expression in response to cardiac stress. We used microarray to examine differential gene expression by Hsp22 deletion at baseline and 3-day pressure overload. Left ventricles from wild type and Hsp22 knockout mice were selected from basal condition (each, n=3) and TAC surgery (each, n=4).
