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Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice.

ABSTRACT: Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. These data show that of new CMs derived from resident c-kitpos eCSCs have a gene expression profile that closely resembles the specific gene expression of adult cardiomyocytes. This result supports a role of c-kitpos eCSCs in the regeneration and repair of myocardial damage. To test the identity and the degree of differentiation of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. Global gene expression profiles by microarray was obtained in c-kitpos eCSCs, c-kitpos eCSC-derived YFPpos CMs and normal adult CMs. c-kitposCD45neg eCSCs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice and harvested at 4th passage (n=3). YFPpos cardiomyocytes were FACS sorted from left ventricle apex of Lentirius-c-kit/cre recombined B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice 28 days after ISO (N=3). Normal adult CMs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice (n=3).

ORGANISM(S): Mus musculus

SUBMITTER: Gianluigi Condorelli

PROVIDER: E-GEOD-49318 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice.

Project description:Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. These data show that of new CMs derived from resident c-kitpos eCSCs have a gene expression profile that closely resembles the specific gene expression of adult cardiomyocytes. This result supports a role of c-kitpos eCSCs in the regeneration and repair of myocardial damage.

2013-07-30 | GSE49318 | GEO

Isoproterenol-induced cardiac hypertrophy trigger proteome remodeling of mouse cardiomyocytes

Project description:Cardiac hypertrophy consists in the enlargement of cardiomyocytes and alteration of the extracellular matrix organization in response to physiological or pathological stress. In pathological hypertrophy ocuurs myocardial damage, loss of cardiomyocytes, fibrosis, inflammation, sarcomere disorganization and metabolic impairment, leading to cardiac dysfunction.The rodent model treated with isoproterenol induces cardiac hypertrophy due the constant activation of β-adrenergic receptors. We conducted a quantitative label-free proteomic analysis of cardiomyocytes isolated from hearts of mice treated or not with isoproterenol to better understand the molecular bases of cellular response due to isoproterenol-induced injury.

2020-05-27 | PXD013020 | Pride

Mus musculus

| PRJNA213626 | ENA

Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction [Array]

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in vitro and in vivo in acute MI. Here we show that in vivo cardiac reprogramming generated iCMs from resident CFs, improved cardiac function, and reversed fibrosis in chronic MI using a novel transgenic mouse system. Transcriptome analysis revealed that in vivo cardiac reprogramming altered the interstitial cell landscape, suppressed signs of fibrosis and inflammation, and activated the angiogenic program. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

2022-12-12 | GSE183932 | GEO

Direct In Vivo Cardiac Reprogramming as a Novel Therapeutic Strategy for Chronic Myocardial Infarction [scRNA-Seq]

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in vitro and in vivo in acute MI. Here we show that in vivo cardiac reprogramming generated iCMs from resident CFs, improved cardiac function, and reversed fibrosis in chronic MI using a novel transgenic mouse system. Single-cell transcriptome analysis revealed that cardiac reprogramming shifted matrix-producing CFs, matrifibrocytes, to a quiescent state and changed the interstitial cell landscape, suppressing fibrotic and inflammatory signatures and activating angiogenic program. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

2022-12-12 | GSE185265 | GEO

Direct in vivo cardiac reprogramming improves cardiac function and ventricular remodeling in chronic MI.

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in acute and chronic MI. Here we show that in vivo cardiac reprogramming improved cardiac function, and reversed cardiac remodeling in chronic MI using a novel transgenic mouse system. Transcriptome analysis revealed that in vivo cardiac reprogramming suppressed signs of fibrosis and inflammation. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

2024-07-01 | GSE240310 | GEO

Differential expression profiles of tsRNAs in myocardial ischemic rats with/without caloric restriction

Project description:We report the application of high-throughput RNA sequencing technology to examine expression profiling of transfer RNA (tRNA)-derived small RNAs (tsRNAs) in a normal control group (Norm group), isoproterenol (ISO)-induced myocardial ischemic group (MI group), and CR-pretreatment plus ISO-induced myocardial ischemic group (CR+MI group). A total of 714 precisely matched tsRNAs were identified in the myocardial tissues from the three groups of rats (701 in Norm, 708 in MI, and 712 in CR+MI). We find that 302 tsRNAs were identified to be notably dysregulated in the MI group: 166 tsRNAs were upregulated while 136 tsRNAs were downregulated compared with those in the Norm group. After CR pretreatment, we identified 136 tsRNAs that were significantly altered compared with those in the MI group: 45 were upregulated while 91 were downregulated. This study provides new ideas for future research on elucidating the mechanisms of CR pretreatment through regulating tsRNAs levels in myocardial ischemic injury.

2020-10-01 | GSE158781 | GEO

Identification of down-stream targets of Notch signaling within the developing mosue kidney collecting ducts.

Project description:Notch signaling deficient kidney collecting ducts may serve as a useful resource to identify principal cell lineage and intercalated lineage specific factors since they develop a reduced number of principal cells and an increased number of intercalated cells compared with wild type kidney collecting ducts. We compared RNA from three E18.5 mouse kidneys per group: HoxB7Cre;RBPJf/-;Rosa+/Eyfp (Notch signaling deficient; mutant) versus RBPJf/f;Rosa+/Eyfp (wild type).

2017-02-27 | GSE68389 | GEO

Metabolism Disorder Promotes Isoproterenol-induced Myocardial Injury in Mice with High Temperature and High Humidity and High-Fat Diet

Project description:<p>Isoproterenol (ISO) provides a simple and non-invasive method for inducing myocardial injury with lower mortality and higher reproducibility. Phlegm-damp syndrome, as known as “Tanshi” in Chinese, is one of Traditional Chinese Medicine (TCM) syndrome differentiation, which plays an important role in the development of cardiovascular diseases. However, the underlying mechanism remains unknown. In our present study, a myocardial injury mouse model was introduced by ISO administration combined with high temperature and high humidity and high fat diet to simulate phlegm-damp syndrome. Nontargeted metabolomics with LC-MS/MS was adopted to reveal serum metabolism profile for elucidating the possible molecular mechanism.</p>

2022-01-10 | MTBLS3886 | MetaboLights

RNA-seq from the hearts of 7-day-old mice that underwent apical resection and anti-arrhythmic drug treatment

Project description:Background: As a biological pump, the heart needs to consume a substantial amount of energy to maintain sustained beating. Myocardial energy metabolism was recently reported to be related to the loss of proliferative capacity in cardiomyocytes (CMs). However, the intrinsic relationship between beating rate and proliferation in CMs and whether energy metabolism can regulate this relationship is not known. In this study, we found that limited heart rate reserve (HRR) induced CM proliferation under physiological conditions and promoted cardiac regenerative repair after myocardial injury. However, the role of HRR in regulating CM proliferation and damaged heart repair has not been explored. Results: We found that the control and isoproterenol groups had more similar transcriptional profiles that clearly differed from those of the five groups treated with each anti-arrhythmic drug and thus were clustered together. With Gene Ontology (GO) analysis, we found that genes that commonly showed upregulated expression in various HRR drug-treated cells were related to proliferation and metabolic regulation, including the cell cycle process, heart process, and nucleoside triphosphate metabolic process, with a particular upregulation of the expression of glucose metabolic genes.

2022-10-23 | GSE186797 | GEO

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