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RNA sequence analysis of hearts tissue after C57BL/6 mice subjected to transverse aortic constriction (TAC) and dioscin treatment

ABSTRACT: To study the differient expression genes, heart tissues from TAC group and TAC treatment with dioscin group are performed to RNA sequence.

ORGANISM(S): Mus musculus

PROVIDER: GSE181347 | GEO | 2023/08/01

REPOSITORIES: GEO

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Gene expression analysis of shUhrf1 cardiomyocytes (CMs) isolated from mice subjected to transverse aortic constriction (TAC) for 1 week

Project description:To identify UHRF1-regulated genes in TAC mice we performed a gene expression analysis of cardiomyocytes (CMs) isolated from mice infected with AVV9 - an adeno-associated viral vector that efficiently transduces cardiomyocytes in vivo-encoding either a scrambled shRNA (AAV9-scr, control group) or sh-Uhrf1 #1 (AAV9-sh-Uhrf1 #1), and subjected to TAC for 1 week.

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Transcriptomic analysis of mice heart following transverse aortic constriction (TAC) surgery

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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.

2013-03-15 | E-GEOD-36407 | biostudies-arrayexpress

RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of mouse hearts to transverse aortic artery constriction (TAC)

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Expression data from mouse heart post transverse aortic constriction (TAC) -surgery 2 weeks

Project description:A number of mediators that have been found to be involved in the pathogenesis of cardiac hypertrophy affecting gene transcription, protein synthesis, metabolism,autophagy, oxidative stress and inﬂammation. These mediators including nuclear transcription factor, microRNAs and long noncoding RNAs. However, the gene expression profiles signaling pathways in the pressure overload-induced cardiac hypertrophy remain unknown. All mice were randomly undertaken sham surgery or TAC for 2 weeks. Hearts were harvested 2 weeks following TAC and performed to further analysis.

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RNA sequence analysis of hearts tissue after C57BL/6 mice subjected to transverse aortic constriction (TAC) and dioscin treatment

Project description:RNA sequence analysis of hearts tissue after C57BL/6 mice subjected to transverse aortic constriction (TAC) and dioscin treatment

| PRJNA751611 | ENA

Gene expression profile of STIM1 deficiency for cardiac remodeling in response to pressure overload by transverse aortic constriction (TAC)

Project description:STIM1 is a Ca2+ sensor of intracellular Ca2+ stores and essentially activates the Ca2+ entry channels of the plasma membrane. STIM1 is predicted to activate transient receptor potential canonical (TRPC) channels and Orai channels, and has a critical role in promoting the development of cardiac hypertrophy. Gene array experiments were performed to analyze the effects of STIM1 deficiency using total RNA from the left ventricles of WT sham, WT TAC, STIM1KO sham and STIM1KO TAC 4 weeks after the operation.

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

2013-03-15 | GSE36407 | GEO

RNA-seq data in cardiac tissues from cardiomyocyte-specific Acsl4 knockout mice after transverse aortic constriction

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2024-08-26 | E-MTAB-14383 | biostudies-arrayexpress

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