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Pressure overload greatly promotes neonatal right ventricular cardiomyocyte proliferation - a new model for heart regeneration study

ABSTRACT: Pressure overload greatly promotes neonatal right ventricular cardiomyocyte proliferation - a new model for heart regeneration study

PROVIDER: PRJNA580253 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10360386_1.fastq.gz	Fastqsanger.gz
	SRR10360386_2.fastq.gz	Fastqsanger.gz
	SRR10360387_1.fastq.gz	Fastqsanger.gz
	SRR10360387_2.fastq.gz	Fastqsanger.gz
	SRR10360388_1.fastq.gz	Fastqsanger.gz

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Pressure overload greatly promotes neonatal right ventricular cardiomyocyte proliferation - a new model for heart regeneration study

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..

2020-08-19 | GSE139561 | GEO

Effect of volume overload on right ventricular remodeling in neonatal SD rats

Project description:We reported the RNAseq analyses of right ventricualr free wall myocardium in neonatal volume overload (VO) SD rat. VO was induced by the fistula between abdominal aorta and inferior vena cava (AVF) within 24 hours postnatally (P1). RNAseq analyses of RV free wall at P7 from VO and sham-operated rat revealed that there were 454 differentially expressed genes between VO and sham group at P7. GO analysis showed that in the VO and sham comparison, the upregulated genes mainly mediated immune system response and the downregulated genes mainly mediated apoptotic process at P7. VO has no effect to neonatal right ventricular cardiomyocyte proliferation.

2021-12-08 | GSE180643 | GEO

The Right Ventricular Fibroblast Secretome Drives Cardiomyocyte Dedifferentiation

Project description:The Right Ventricular Fibroblast Secretome Drives Cardiomyocyte Dedifferentiation

| PRJNA552980 | ENA

Effect of neonatal right ventricular pressure overload on gene expression and regions of open chromatin during postnatal heart development

Project description:To investigate the effect of pressure overload (PO) during postnatal right ventricular (RV) development, we established the RV PO model by conducting pulmonary artery banding (PAB) surgery on neonatal Sprague-Dawley (SD) rats. We then performed gene expression and chromatin openness profiling analysis using data obtained from RNA-seq and ATAC-seq of RV free walls from PO and sham-operated rats at postnatal day 21 (P21).

2024-05-17 | GSE210180 | GEO

Transcriptomic and Functional Analyses of Mitochondrial Dysfunction in Pressure Overload-induced Right Ventricular Failure

Project description:Transcriptomic and Functional Analyses of Mitochondrial Dysfunction in Pressure Overload-induced Right Ventricular Failure

| PRJNA639270 | ENA

Time dependence of volume overload on right ventricular remodeling during preadolescence

Project description:Time dependence of volume overload on right ventricular remodeling during preadolescence

| PRJNA661200 | ENA

Cyclosporin ameliorates right ventricular remodeling of postnatal mice with volume overload.

Project description:Cyclosporin ameliorates right ventricular remodeling of postnatal mice with volume overload.

| PRJNA1069016 | ENA

Single-cell RNA-sequencing reveals the effects of right ventricular volume overload on cardiomyocyte proliferation via immune responses

Project description:Single-cell RNA-sequencing reveals the effects of right ventricular volume overload on cardiomyocyte proliferation via immune responses

| PRJNA1073434 | ENA

Effect of volume overload on right ventricular remodeling in neonatal SD rats

Project description:Effect of volume overload on right ventricular remodeling in neonatal SD rats

| PRJNA749019 | ENA

Dynamic adaptation of myocardial proteome during heart failure development after induction of left ventricular pressure overload in mice

Project description:We analyzed time dependent global proteomic adaptations during heart failure (HF) progression in a mouse model, suffering from left ventricular pressure overload due to transverse aortic constriction (TAC), to gain deeper insights in the disease development and identify new biomarker candidates. The hearts from TAC and sham mice were examined by cardiac MRI on either day 4, 14, 21, 28, 42, and 56 after surgery (n=6 group/time point). At each time point, proteomes of the left (LV) and right ventricles (RV) of TAC and sham mice were analyzed by mass spectrometry (MS).

2018-07-16 | PXD007171 | Pride

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