CITED4 is Required for Exercise-induced Cardiac Growth and Cardiomyogenesis in Mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA952256 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24067172_1.fastq.gz | Fastqsanger.gz | |||
| SRR24067172_2.fastq.gz | Fastqsanger.gz | |||
| SRR24067173_1.fastq.gz | Fastqsanger.gz | |||
| SRR24067173_2.fastq.gz | Fastqsanger.gz | |||
| SRR24067174_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:To investigate the role of CITED4 in heart in exercise, we generated cardiomyocyte-specific CITED4 knockout (KO) by crossing CITED4 flox/flox (Flox) mice with aMHC-Cre mice and subjected them to either sedentary or exercise for eight weeks. We then performed gene expression profiling analysis using data obtained from RNA-seq.
2025-04-03 | GSE228969 | GEO
Project description:The heart grows in response to pathological and physiological stimuli, while the former often precedes cardiomyocyte loss and heart failure, the latter paradoxically protects the heart and enhances cardiomyogenesis. Long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis. The purpose of this study was to compare transcriptome profilings in exercise-induced physiological cardiac growth and stress-induced pathological cardiac growth. We identified a set of lncRNAs called long noncoding exercise associated cardiac transcripts (lncExACT). One of them, lncExACT1, whose cardiac expression was downregulated after exercise but upregulated after transverse aortic constriction. Inhibition of lncExACT1 induced physiolgoical cardiac growth while overexpression of lncExACT1 induced pathological hypertrophy and heart failure.
2022-10-18 | GSE186081 | GEO
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.
2020-04-30 | GSE149584 | GEO
Project description:Comparative analysis of mouse cardiac left ventricle gene expression: voluntary wheel exercise and pregnancy-induced cardiac hypertrophy We performed microarray analysis on RNA from left ventricles of mice in non-pregnant diestrus cycle, mid-pregnancy (MP), late-pregnancy (LP), and immediate post-partum (0PP). These were compared to 7days (7EX) and 21 days (21EX) of voluntary wheel running exercise.
2012-03-08 | E-GEOD-36330 | biostudies-arrayexpress
Project description:During acute sympathetic stress, the overeactivation of β-adrenergic receptors (β-ARs) caused cardiac fibrosis, by triggering inflammation and cytokine expression. It is unknown whether exercise training inhibited acute β-AR overactivation-induced cytokine expression and cardiac injury. Here, we reported that running exercise inhibited cardiac fibrosis and improved cardiac function in mice treated by isoproterenol, a β-AR agonist. Cytokine antibody array revealed that exercise prevented the expression changes of most cytokines induced by isoproterenol. Specifically, 18 ISO-upregulated and 3 ISO-downregulated cytokines belonged to six families (eg. chemokine) were prevented. A further KEGG analysis of these cytokines revealed that Hedgehog and Rap1 signaling pathways were involved in the regulation of cytokine expression by exercise. The expression changes of some cytokines that were prevented by exercise were verified by ELISA and real-time PCR. In conclusion, running exercise prevented the cytokine changes following acute β-AR overactivation and therefore attenuated cardiac fibrosis.
2019-03-30 | GSE129022 | GEO
Project description:Comparative analysis of mouse cardiac left ventricle gene expression: voluntary wheel exercise and pregnancy-induced cardiac hypertrophy
2012-03-08 | GSE36330 | GEO
Project description:Physical exercise is a cornerstone for preventing diet-induced obesity, while it is unclear whether physical exercise could offset high-fat, high-calories diet (HFCD)-induced cardiac dysfunction. Here, mice were fed with HFCD and simultaneously subjected to physical exercise. As expected, physical exercise prevented HFCD-induced whole-body fat deposition. However, physical exercise exacerbated HFCD-induced cardiac damage. Further metabolomic analysis results showed that physical exercise induced circulating lipid redistribution, leading to excessive cardiac lipid uptake and lipotoxicity. Our study provides valuable insights into the cardiac effects of exercise in mice fed with HFCD, suggesting that counteracting the negative effect of HFCD by simultaneous physical exercise might be detrimental. Moreover, inappropriate physical exercise may damage certain organs even though it leads to weight loss and overall metabolic benefits. Of note, the current findings are based on animal experiments, the generalizability of these findings beyond this specific diet and mouse strain remains to be further explored.
2024-11-30 | PXD058460 |
Project description:Physiological exercise leads to an activation of an distinct genetic program in the heart. During this process, we identified histone deacetlyase 4 (HDAC4) as an epigentic modifier, that regulates this adaptive process. To identify HDAC4 dependent genes that can are regulated after physiological stress, we investigated the cardiac gene expression in cardiomyocyte specific HDAC4 knockout animals and control animals after running exercise. We used microarrays to detail the global programme of gene expression underlying physiological cardiac adaption on exercise and identified distinct, histone deacetylase 4 dependent up-regulated genes during this process.
2017-06-07 | GSE72900 | GEO
Project description:During exercise there is a site-specific increase in ROS within muscle required for the beneficial adaptive response by activation of specific signalling pathways. Peroxiredoxin 2 (Prdx2), an abundant cytoplasmic 2-Cys peroxidase, is required for the adaptive beneficial hormesis response to H2O2, myoblasts with knockdown of Prdx2 did not increase mitochondrial content and had disrupted myogenesis. Using a 5-day swimming protocol in C. elegans, previously been demonstrated to improve healthspan, we observed increased mitochondrial content, fitness, survival and longevity in wild type (N2) worms. However, prdx-2 mutant worms had decreased fitness, disrupted mitochondria, reduced survival and lifespan following exercise. Global proteomics following exercise revealed an increase in the abundance of proteins involved in fatty oxidation and ion transport, decrease in proteins involved in cuticle formation in N2 worms. In the prdx-2 mutants following exercise there was an increase in proteins related to the mTOR pathway and decrease in transsulfuration and microRNA biogenesis proteins. Relative quantification of the reversible oxidation state of individual Cysteine (Cys) residues revealed an increased oxidation of specific Cys residues following exercise in prdx-2 mutant. A number of regulatory Cys residues of metabolic, cytoskeletal and calcium handling proteins are reduced in N2 worms. A redox signalling relay whereby the oxidative equivalents from ROS are transferred from evolutionary conserved Prdxs to target proteins, would confer specificity on redox signalling required for the beneficial adaptations to exercise.
2023-03-11 | PXD037698 | Pride
Project description:Endothelium in embryonic hematopoietic tissues generates hematopoietic stem/progenitor cells; however, it is unknown how its unique potential is specified. We show that transcription factor Scl/Tal1 is essential for both establishing the hematopoietic transcriptional program in hemogenic endothelium and preventing its misspecification to a cardiomyogenic fate. Scl-/- embryos activated a cardiac transcriptional program in yolk sac endothelium, leading to the emergence of CD31+Pdgfrα+ cardiogenic precursors that generated spontaneously beating cardiomyocytes. Ectopic cardiogenesis was also observed in Scl-/- hearts, where the disorganized endocardium precociously differentiated into cardiomyocytes. Induction of mosaic deletion of Scl in Sclfl/flRosa26Cre-ERT2 embryos revealed a cell-intrinsic, temporal requirement for Scl to prevent cardiomyogenesis from endothelium. Scl-/- endothelium also upregulated the expression of Wnt antagonists, which promoted rapid cardiomyocyte differentiation of ectopic cardiogenic cells. These results reveal unexpected plasticity in embryonic endothelium such that loss of a single master regulator can induce ectopic cardiomyogenesis from endothelial cells.
2012-08-03 | GSE27445 | GEO