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Transcriptional regulation patterns revealed by high-resolution chromatin immunoprecipitation during cardiac hypertrophy

ABSTRACT: Purpose: To identify the differential transcriptional patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Results: Our data revealed novel transcriptional patterns during cardiac growth conditions. The results showed that most of the essential genes are regulated by promoter clearance of paused RNA pol II, while de novo recruitment is required for regulation of mostly speclaized genes during cardiac growth. We have identified two major modes of gene regulation durign cardiac hypertrophy and four transcriptional growth patterns. The results are published in January 2013 issue of Journal of Biological Chemistry.

ORGANISM(S): Mus musculus

PROVIDER: GSE50637 | GEO | 2013/09/06

SECONDARY ACCESSION(S): PRJNA218141

REPOSITORIES: GEO

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Transcriptional regulation patterns revealed by high-resolution chromatin immunoprecipitation during cardiac hypertrophy

Project description:Purpose: To identify the differential transcriptional patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Results: Our data revealed novel transcriptional patterns during cardiac growth conditions. The results showed that most of the essential genes are regulated by promoter clearance of paused RNA pol II, while de novo recruitment is required for regulation of mostly speclaized genes during cardiac growth. We have identified two major modes of gene regulation durign cardiac hypertrophy and four transcriptional growth patterns. The results are published in January 2013 issue of Journal of Biological Chemistry. Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for RNA polII and H3K9ac- ChIP-Seq.

2013-09-06 | E-GEOD-50637 | biostudies-arrayexpress

Genome wide TFIIB binding during postnatal and pressure-induced cardiac hypertrophy

Project description:Purpose: To identify the differential TFIIB bindingl patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq. Results: In accordance with previosly published data (Sayed D, et. al. JBC, 2013 Jan 25;288(4):2546-58) with genome wide polII and H3K9ac status during cardiac hypertrophy (GSE50637), Denovo TFIIB recruitment was restricted to speclaized genes with cardiac hypertrophy.

2014-11-17 | GSE56813 | GEO

Genome wide TFIIB binding during postnatal and pressure-induced cardiac hypertrophy

2014-11-17 | E-GEOD-56813 | biostudies-arrayexpress

miRNA-99 family diverges physiological cardiac hypertrophy to pathological cardiac hypertrophy

Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (Î±-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of Î±-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon Î±-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure. Small RNA profiles of control and hypertrophied cardiomyocyte H9c2 cells were generated by deep sequencing using Illumina HiSeq 2000

2015-11-01 | E-GEOD-73597 | biostudies-arrayexpress

Whole-transcriptome analysis identifies re-expression of fetal splice variants in cardiac hypertrophy

Project description:Cardiac hypertrophy has been well-characterized at the level of transcription. During cardiac hypertrophy, genes normally expressed primarily during fetal heart development are re-expressed, and this fetal gene program is believed to be a critical component of the hypertrophic process. Recently, alternative splicing of mRNA transcripts has been shown to be temporally regulated during heart development, leading us to consider whether fetal patterns of splicing also reappear during hypertrophy.We hypothesized that patterns of alternative splicing occurring during heart development are recapitulated during cardiac hypertrophy. Here we present a whole-transcriptome study of isoform expression during pressure-overload cardiac hypertrophy induced by 10 days of transverse aortic constriction (TAC) in rats and in developing fetal rat hearts compared to sham-operated adult rat hearts, using high-throughput sequencing of poly(A) tail mRNA. Quantification of isoform expression in fetal rat hearts, pressure-overloaded rat hearts, and sham-operated rat hearts by Illumina GAIIx in triplicate

2013-05-14 | E-GEOD-42411 | biostudies-arrayexpress

Whole-transcriptome analysis identifies re-expression of fetal splice variants in cardiac hypertrophy

2013-05-14 | GSE42411 | GEO

Transcriptome analysis of mouse cardiac hypertrophy

Project description:RNA-Seq analysis of mouse cardiac transcriptome. Transverse aortic contraction was used to induce cardiac hypertrophy (TAC). To compare wild type and physiological cardiac hypertrophy 'Sendetary' (feeding mouse during 4 weeks) and 'Swim (exercise training to induce the cardiac hypertrophy) samples were analysed.

2012-05-11 | E-MTAB-727 | biostudies-arrayexpress

miRNA-99 family diverges physiological cardiac hypertrophy to pathological cardiac hypertrophy

Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (α-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of α-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon α-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure.

2015-11-01 | GSE73597 | GEO

Regression of Post-Prandial Cardiac Hypertrophy in Burmese Pythons is Mediated by FoxO1

Project description:As ambush-hunting predators that consume large prey after long intervals of fasting, Burmese pythons evolved with unique adaptations for regulating organ structure and function. Among these is cardiac hypertrophy that develops within three days following a meal (1, 2), which we previously showed was initiated by circulating growth factors (3). Post-prandial cardiac hypertrophy in pythons also rapidly regresses with subsequent fasting (2); however, the molecular mechanisms that regulate the dynamic cardiac remodeling in pythons during digestion are largely unknown. In this study, we employed a multi-omics approach coupled with targeted molecular analyses to examine remodeling of the python ventricular transcriptome and proteome throughout digestion. We found that forkhead box protein O1 (FoxO1) signaling was suppressed prior to hypertrophy development and then activated with regression, which coincided with decreased and then increased expression, respectively, of FoxO1 transcriptional targets involved in protein degradation. To define the molecular mechanistic role of FoxO1 in hypertrophy regression, we used cultured mammalian cardiomyocytes treated with post-fed python plasma. Hypertrophy regression both in pythons and in vitro coincided with activation of FoxO1-dependent autophagy; however, introduction of a FoxO1-specific inhibitor prevented both regression of cell size and autophagy activation. Finally, to determine if FoxO1 activation could induce regression, we generated an adenovirus expressing a constitutively active FoxO1. FoxO1 activation was sufficient to prevent and reverse post-fed plasma-induced hypertrophy, which was partially prevented by autophagy inhibition. Our results indicate that modulation of FoxO1 activity contributes to the dynamic ventricular remodeling in post-prandial Burmese pythons.

2024-09-12 | PXD054079 | Pride

The effect of age on the skeletal muscle transcriptome during hypertrophy

Project description:Transcriptome analysis of skeletal muscle during hypertrophic growth in aged mice Global gene expression patterns were determined from microarray results on day 1, 3, 5, 7, 10 and 14 during plantaris muscle hypertrophy induced by synergist ablation in old adult mice (25 months).

2015-06-01 | GSE67160 | GEO

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