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RNA sequencing analyses of grl/hey2-overexpressing hearts and control hearts, as well as grl/hey2-deficient hearts and wild-type hearts following ventricular resection at 7 dpa

ABSTRACT: As Grl/Hey2 directly binds DNA through E box motifs and mediates transcription repression, we aim to gain insights into potential target genes of Grl/Hey2 during heart regeneration. We performed RNA-seq analyses using total RNAs collected from 4-HT-treated Tg(cmlc2:creER;cmlc2:nRSGG) hearts and Tg(cmlc2:nRSGG) control hearts, as well as grl5nt-/- mutant hearts and wild-type hearts following ventricular resection at 7 dpa. Using RNA profile analyses, we have identified some potential genes act downstream of Grl/Hey2-dependent transcriptional repression during heart regeneration.

ORGANISM(S): Danio rerio

PROVIDER: GSE129499 | GEO | 2020/09/14

REPOSITORIES: GEO

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RNA sequencing analyses of grl/hey2-overexpressing hearts and control hearts, as well as grl/hey2-deficient hearts and wild-type hearts following ventricular resection at 7 dpa

Project description:RNA sequencing analyses of grl/hey2-overexpressing hearts and control hearts, as well as grl/hey2-deficient hearts and wild-type hearts following ventricular resection at 7 dpa

| PRJNA531508 | ENA

CHF1/Hey2 Promotes Physiological Hypertrophy in response to Pressure Overload

Project description:We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways.

2010-01-20 | GSE13031 | GEO

Transcription profiling of mouse treated by ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium reveals CHF1/Hey2 promotes physiological hypertrophy in response to pressure overload

2010-02-17 | E-GEOD-13031 | biostudies-arrayexpress

Transcription Factor CHF1/Hey2 Regulates Specific Gene Sets in Serum Stimulated Primary Cardiac Myocytes

Project description:Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChipÂ® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy. Transgenic Mice and Neonatal Mouse Myocyte Culture: WT no serum, 5; WT with serum, 7; TG no serum, 6; TG with serum, 7.

2010-04-08 | E-GEOD-14288 | biostudies-arrayexpress

Site-specific N-glycan Analysis of Neonatal Mouse Hearts

Project description:The heart of a newborn mouse has an exceptional capacity to regenerate from myocardial injury but lose it after a week of life, which has been utilized as a valuable model to explore the cues for heart regeneration. More and more researches indicated that glycoprotein played an important role in cardiac regeneration. Elucidating the glycosylation processes associated with heart regeneration will be beneficial for the molecular mechanism studies of heart regeneration as well as discovery of potential therapeutic strategies for human cardiac diseases. In this work, an integrated glycoproteomic and proteomic analysis were performed to investigate the differences in glycoprotein abundances and site-specific glycosylation occupancy between neonatal day 1 (P1) and day 7 (P7) of mouse hearts. The intact glycoepeptides were enriched and identified in both P1 and P7 hearts. To screen for differentially regulated glycoproteins, we compared the expression levels of intact glycopeptides between P1 and P7 hearts using label free quantification. Eventually, the glycosylation occupancy of site-specific N-glycans were obtained by comparing the alterations of intact glycopeptides with their corresponding protein expression levels obtained from global proteomic analysis. These altered glycosylation patterns among proteins between P1 and P7 mouse hearts have a significant potential to aid our understanding of the regenerative capacity loss in neonatal mouse hearts during the first week, thus leading to novel therapeutic approaches to recover the capacity.

2020-05-26 | PXD017139 | Pride

Next Generation Sequencing Facilitates Quantitative Analysis of Tg(hsp70:dn-xBrg1) and wild-type sibling hearts Transcriptomes

Project description:The goal of this study is to compare the NGS-derived heart transcriptome profiling (RNA-seq) between Tg(hsp70:dn-xBrg1) and wild-type sibling injured hearts.

2017-08-13 | GSE81627 | GEO

Whole genome microarray gene expression profiling of transgenic mouse hearts with four-fold increased BBLN contents

Project description:The study performed whole genome microarray gene expression profiling of mouse hearts from BBLN-transgenic mice with four-fold increased cardiac BBLN (Bublin coiled coil protein) contents (Tg-BBLN-low) in comparison to non-transgenic FVB hearts. Tg-BBLN-low mice with four-fold increased cardiac BBLN expression under control of the myocardium-specific alpha-MHC promoter developed features of compensated heart failure with increasing age, which was characterized by a significantly reduced left ventricular ejection fraction as determined by echocardiography. To investigate the compensated heart failure phenotype of Tg-BBLN-low mice, whole genome micoarray gene expression profiling was performed. The microarray data show that moderately increased cardiac BBLN levels are sufficient to induce features of pathological cardiac remodeling.

2023-09-18 | GSE241030 | GEO

Gene expression changes in beta-blocker treated neonatal hearts

Project description:The regeneration potential of the mammalian heart is limited. We found that treatment of beta-blocker robustly enhanced cardiomyocyte proliferation and promoted cardiac regeneration post myocardial infarction. To investigate the gene expression changes, we performed RNA-seq using the hearts treated with beta-blocker for 7 days.

2022-08-30 | GSE186099 | GEO

Expression data from neonatal heart after apex resection

Project description:Apical resection in 1-day-old mice results in complete regenerated heart and normal cardiac function, which is characterized by significant cardiomyocyte proliferation with minimal fibrosis. Local damage on hearts of 1-day-old mice can amplify cardiomyocyte proliferation located in the whole ventricle rather than limited damage area. This response provides a reasonable screening model to identify novel genes involved in endogenous cardiac regeneration

2020-07-10 | GSE154071 | GEO

Single nucleus RNA-seq of cardiomyocytes from neonatal mouse hearts after injury

Project description:The adult mammalian heart is incapable of regeneration following injury. In contrast, the neonatal mouse heart can efficiently regenerate during the first week of life. The molecular mechanisms that mediate the regenerative response and its blockade in later life are not understood. Here, by single-nucleus RNA sequencing, we map the dynamic transcriptional landscape of five distinct cardiomyocyte populations in healthy, injured and regenerating mouse hearts. We identify immature cardiomyocytes that enter the cell-cycle following injury and disappear as the heart loses the ability to regenerate. These proliferative neonatal cardiomyocytes display a unique transcriptional program dependent on NFYa and NFE2L1 transcription factors, which exert proliferative and protective functions, respectively. Cardiac overexpression of these two factors conferred protection against ischemic injury in mature mouse hearts that were otherwise non-regenerative. These findings advance our understanding of the cellular basis of neonatal heart regeneration and reveal a transcriptional landscape for heart repair following injury.

2020-03-18 | GSE130699 | GEO

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