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MiRNA expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

ABSTRACT: miRNA expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

PROVIDER: PRJNA631727 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11770289.fastq.gz	Fastqsanger.gz
	SRR11770290.fastq.gz	Fastqsanger.gz
	SRR11770291.fastq.gz	Fastqsanger.gz
	SRR11770292.fastq.gz	Fastqsanger.gz
	SRR11770293.fastq.gz	Fastqsanger.gz

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Gene expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

Project description:Rationale: Cardiac CITED4 is induced by exercise and is sufficient to cause physiological hypertrophy and mitigate adverse ventricular remodeling after ischemic injury. However, the role of endogenous CITED4 in response to physiological or pathological stress is unknown. Objective: To investigate the role of CITED4 in murine models of exercise and pressure overload. Methods and Results: We generated cardiomyocyte-specific CITED4 knockout mice (C4KO) and subjected them to an intensive swim exercise protocol as well as transverse aortic constriction (TAC). Echocardiography, western blotting, qPCR, immunohistochemistry, immunofluorescence, and transcriptional profiling for mRNA and miRNA expression were performed. Cellular crosstalk was investigated in vitro. CITED4 deletion in cardiomyocytes did not affect baseline cardiac size or function in young adult mice. C4KO mice developed modest cardiac dysfunction and dilation in response to exercise. After TAC, C4KOs developed severe heart failure with left ventricular dilation, impaired cardiomyocyte growth accompanied by reduced mammalian target of rapamycin (mTOR) activity and maladaptive cardiac remodeling with increased apoptosis, autophagy, and impaired mitochondrial signaling. Interstitial fibrosis was markedly increased in C4KO hearts after TAC. RNAseq revealed induction of a pro-fibrotic miRNA network. miR30d was decreased in C4KO hearts after TAC and mediated crosstalk between cardiomyocytes and fibroblasts to modulate fibrosis. miR30d inhibition was sufficient to increase cardiac dysfunction and fibrosis after TAC. Conclusions: CITED4 protects against pathological cardiac remodeling by regulating mTOR activity and a network of miRNAs mediating cardiomyocyte to fibroblast crosstalk. Our findings highlight the importance of CITED4 in response to both physiological and pathological stimuli.

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Gene expression data from CITED4 knockout and control mouse hearts after transverse aortic constriction

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Project description:Hearts(left ventricles) were harvested from control wildtype and ISG15 knockout mice and wildtype and ISG15 knockout mice 4 weeks after pressure overload induced by transverse aortic constriction. Nano LC-MS/MS analysis was performedon left ventricle tissue following protein extraction, trypsin digestion, peptide desalting, anti K-e-GG enrichment.

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Transcription profiling of hearts from FVB male mice subjected to cardiac pressure overload by transverse aortic constriction to study the quantitative relationships between gene expression and left ventricular hypertrophy

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The effect of transverse aortic constriction on gene expression in Balb/cJ versus Balb/cByJ(∆ACADS) mice hearts

Project description:RNA-Seq data show that ACADS knockout curbs gene expression after transverse aortic constriction in mice

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mRNA Expression data from transverse aortic constriction hearts (cardiovascular disease) and sham hearts in mice.

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mRNA Expression data from transverse aortic constriction hearts (cardiovascular disease) and sham hearts in mice.

Project description:We used transverse aortic constraction pressure overload hypertrophy mouse hearts as a model of cardiovascular disease to study the genetic changes between TAC and SHAM (normal) mouse hearts and over 1 circadian cycle (24h). This is one approach to identify diurnal genetic biomarkers of cardiovascular disease. The micorarray approach allowed to see the gene expression in all genes in cardiovascular disease and sham hearts. There are 36 samples of cardiovascular disease (TAC) and normal SHAM hearts. For TAC: There were 3 mice sacrificed at each time point as biological replicates, for 6 timepoints over 24 hrs. For SHAM: There were 3 mice sacrificed at each time point as biological replicates, for 6 timepoints over 24 hrs.

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