Heart transcriptional changes with prednisone with inducible cardiomyocyte-specific KLF15 ablation
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ABSTRACT:
PROVIDER: PRJNA1062831 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:this dataset encompasses the cardiac transcriptomic changes elicited in myocardial tissues of 4months-old mice at 4 hours after a single ZT0 prednisone (1mg/kg i.p.) injection, or vehicle, in cardiomyocyte-KLF15-WT versus cardiomyocyte-KLF15-KO conditions (inducible, tamoxifen-driven ablation right prior to drug pulse).
2024-01-13 | GSE252857 | GEO
Project description:this dataset encompasses the cardiac transcriptomic changes elicited in myocardial tissues of 4months-old male mice at 4 hours after a single ZT0 prednisone (1mg/kg i.p.) injection, or vehicle, in cardiomyocyte-GR-WT versus cardiomyocyte-GR-KO conditions (inducible, tamoxifen-driven ablation right prior to drug pulse).
2024-01-13 | GSE252826 | GEO
Project description:Heart transcriptional changes with prednisone with inducible cardiomyocyte-specific GR ablation
| PRJNA1062780 | ENA
Project description:this dataset encompasses the cardiac KLF15 epigenomic changes elicited in 4-month-old mice with a single ZT0 prednisone (1mg/kg i.p.) injection
2024-01-31 | GSE254114 | GEO
Project description:Myocardial KLF15 epigenomic changes with single ZT0 prednisone pulse
| PRJNA1068584 | ENA
Project description:Sustained cardiac stress promotes the transition from an adaptive response to heart failure. Understanding of mechanisms governing this transition will assist in identifying targets that prevent this progression. Our study revealed age-specific transcriptional functions mediated by KLF15 that are crucial for cardiac homeostasis. We report that postnatally, KLF15 continuously activates cardiac metabolism, but represses pathological, hypertrophic pathways associated with cardiomyocyte de-differentiation and endothelial cell (EC) remodeling in an age-dependent manner. Our integrative genomic and transcriptomic analyses identified novel target genes directly bound, and either activated or repressed by KLF15 in vivo in the adult heart. We identified a cooperative program inducing aberrant EC remodeling, caused by a reduction of KLF15 and a concomitant activation of Wnt signaling. Within this program, we further identified a so far uncharacterized cardiac gene - Shisa3, which is expressed in the developing heart and is upregulated in cardiac hypertrophy, ischemia and failure. Importantly, we demonstrate that the KLF15- and Wnt co-dependent, SHISA regulation occurs also in the human myocardium. Altogether, our results unraveled and characterized a previously unknown cardiac gene Shisa3, and attributed its significance to EC homeostasis of the adult heart, controlled by KLF15-Wnt dynamics. Purpose: The aim of this study was to compare transcriptome profiles (RNA-seq) of heart tissue with a WT or KO Klf15 locus at different murine ages - postnatal day10 (p10), 4-week-old and 20-week-old mice. Methods: Cardiac tissue total RNA profiles for different groups were obtained using deep sequencing, in triplicates, using Illumina HiSeq4000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat, followed by DESeq2. qPCR validation was performed using TaqMan and SYBR Green assays. Conclusions: Our study represents the first detailed analysis of the processes triggered upon Klf15 loss in hearts of different murine postnatal ages, which was so far not investigated. We report that this Klf15 loss first triggers Wnt canonical pathway activation, followed by activation of the non-canonical Wnt components, culminating in heart failure.
2019-10-07 | GSE113027 | GEO
Project description:Background: Genomic and experimental studies suggest a role for PITX2 in atrial fibrillation (AF). To assess whether this association is relevant for recurrent AF in patients, we tested whether left atrial PITX2 affects recurrent AF after AF ablation. Methods: mRNA concentrations of PITX2 and its cardiac isoform, PITX2c, were quantified in left atrial appendages (LAA) from patients undergoing thoracoscopic AF ablation, either in whole LAA tissue (n=83) or in LAA cardiomyocytes (n=52), and combined with clinical parameters to predict AF recurrence. Literature suggests bone morphogenetic protein 10 (BMP10) as a PITX2-repressed, atrial-specific, secreted protein. BMP10 plasma concentrations were combined with eleven cardiovascular biomarkers and clinical parameters to predict recurrent AF after catheter ablation in 359 patients. Results: Reduced cardiomyocyte PITX2 concentrations, but not whole LAA tissue PITX2, were associated with AF recurrence after thoracoscopic AF ablation (16% decreased recurrence per 2-(ΔΔCt) increase in PITX2). RNA sequencing, qPCR and Western blotting confirmed BMP10 as one of most PITX2-repressed atrial genes. Left atrial size (hazard ratio per mm increase, HR [95%CI] 1.055 [1.028, 1.082], non-paroxysmal AF (HR 1.672 [1.206, 2.318]) and elevated BMP10 (HR 1.339 [CI 1.159, 1.546] per quartile increase) were predictive of recurrent AF. BMP10 outperformed eleven other cardiovascular biomarkers in predicting recurrent AF. Conclusions: Reduced left atrial cardiomyocyte PITX2 and elevated plasma concentrations of the PITX2-repressed, secreted, atrial protein BMP10 identify patients at risk of recurrent AF after ablation.
2020-06-19 | GSE152181 | GEO
Project description:By comparing the ChIPseq signal of REV_ERBa in control (Flox) and cardiomyocytic KLF15 knockout (cKO), we identified the KLF15 dependent REV-ERBa binding and repression in the heart. We further compared the differential binding sites to KLF15 binding site, using a FLAG tagged cardiomyocytic transgenic (cTG1) mice.
2015-12-30 | GSE73741 | GEO
Project description:The objective of this study was to dertemine GR binding patterns within wild type murine embryonic fibroblasts in comparison to embryonic fibroblasts derived from mice containing a null mutation for Klf15. This study utilized duplicate samples and the following conditions. Wild type cells treated with ethanol (pooled single sample secondary to low starting material); wild type cells treated with dexamethasone for 1 hour (2 samples); Klf15-/- cells treated with ethanol (2 samples); Klf15 -/- cells treated with dexamethasone (2 samples). Samples treated with ethanol served as controls.
2015-06-18 | E-GEOD-69947 | biostudies-arrayexpress