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Gene expression profiling of cardiomyocyte-enriched populations isolated from mice subject to transverse aortic constriction (TAC) and treated with BIX-01294 for 1 week

ABSTRACT: The role of the histone mehyltrasferase G9a (also known as Ehmt2) in cardiac hypertrophy has not been studied extensively. To address how G9a promotes cardiac hypertrophy, we assessed the gene expression signature defined by G9a in cardiomyocytes (CM) of mice subject to transverse aortic constriction (TAC) for 1 wk, a surgical procedure that causes cardiac hypertrophy following the induction of pressure overload. To this end, we compared the expression profiles of CMs isolated from mice treated with the G9a inhibitor BIX-01294 and control groups (untreated and DMSO-treated mice at baseline and after TAC). The expression profiles were defined by Illumina arrays .

ORGANISM(S): Mus musculus

PROVIDER: GSE93691 | GEO | 2017/08/30

SECONDARY ACCESSION(S): PRJNA361564

REPOSITORIES: GEO

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Expression data from mouse heart post transverse aortic constriction (TAC) -surgery 2 weeks

Project description:A number of mediators that have been found to be involved in the pathogenesis of cardiac hypertrophy affecting gene transcription, protein synthesis, metabolism,autophagy, oxidative stress and inﬂammation. These mediators including nuclear transcription factor, microRNAs and long noncoding RNAs. However, the gene expression profiles signaling pathways in the pressure overload-induced cardiac hypertrophy remain unknown. All mice were randomly undertaken sham surgery or TAC for 2 weeks. Hearts were harvested 2 weeks following TAC and performed to further analysis.

2021-08-24 | GSE127954 | GEO

Gene expression profile of STIM1 deficiency for cardiac remodeling in response to pressure overload by transverse aortic constriction (TAC)

Project description:STIM1 is a Ca2+ sensor of intracellular Ca2+ stores and essentially activates the Ca2+ entry channels of the plasma membrane. STIM1 is predicted to activate transient receptor potential canonical (TRPC) channels and Orai channels, and has a critical role in promoting the development of cardiac hypertrophy. Gene array experiments were performed to analyze the effects of STIM1 deficiency using total RNA from the left ventricles of WT sham, WT TAC, STIM1KO sham and STIM1KO TAC 4 weeks after the operation.

2014-07-01 | E-GEOD-38733 | biostudies-arrayexpress

The genomic distribution of G9a, H3K9me2 and H3K27me3 in cardiac hypertrophy.

Project description:The role of the histone methyltrasferase G9a (also known as Ehmt2) in the normal heart has not been studied extensively. To identify which genes were direct targets of G9a in hypertrophic cardiomyocytes, we performed ChIP-seq for G9a and H3K9me2 – the main histone methylation catalysed by the HMT – on cardiomyocytes isolated from normal mice (sham) and mice subject to transverse aortic constriction (TAC) for 1 wk, a surgical procedure that causes cardiac hypertrophy following the induction of pressure overload. We considered the best G9a-bound genomic regions as those in which G9a and H3K9me2 peaks overlapped. Since G9a contributes to trimethylation of H3K27 at a set of developmental genes through its interaction with PRC2, we also evaluated whether G9a had an effect on the distribution of this histone mark in hypertrophic cardiomyocytes. To this end, we performed ChIP-seq for H3K27me3 in CMs isolated from sham and TAC mice.

2017-08-30 | GSE93752 | GEO

Deletion of cardiac-enriched lncRNA CARDINAL exacerbate TAC induced hypertrophy

Project description:Pathological cardiac hypertrophy is featured by enhanced protein synthesis. Translation inhibition is effective in treating cardiac hypertrophy, yet with systematic side effect. We identified a cardiac-enriched LncRNA CARDINAL, when deleted, exacerbate transaortic constriction (TAC) induced hypertrophy.

2024-04-22 | GSE210982 | GEO

AAV9-medated cardiac expression of lncRNA CARDINAL ameliorate TAC induced hypertrophy

Project description:Pathological cardiac hypertrophy is featured by enhanced protein synthesis. Translation inhibition is effective in treating cardiac hypertrophy, yet with systematic side effect. We identified a cardiac-enriched LncRNA CARDINAL, when over-expressed in cardiomyocyte using AAV9 driven by cTNT promoter, ameliorate transaortic constriction (TAC) induced hypertrophy.

2024-04-22 | GSE210983 | GEO

The G9a histone methyltransferase inhibitor BIX-01294 modulates gene expression during gametocyte development and transmission

Project description:Transmission of the malaria parasite Plasmodium falciparum from the human to the mosquito is initiated by sexual precursor cells, the gametocytes. Gametocytes are formed in response to stress signals and following up-take by a blood-feeding Anopheles mosquito initiate sexual reproduction. Gametocytes need to fine tune their gene expression in order to develop inside the mosquito to continue life-cycle progression. Previously we showed that post-translational histone acetylation controls gene expression during gametocyte development and transmission. However, the role of histone methylation remains poorly understood. We here use the histone G9a methyltransferase inhibitor BIX-01294 to investigate the role of histone methylation in regulating gene expression in gametocytes. Growth assays demonstrated that BIX-01294 inhibits intraerythrocytic replication with an IC50 of 13.0 nM. Furthermore, BIX-01294 significantly impairs gametocyte maturation and reduces the formation of gametes and zygotes. Comparative transcriptomics between BIX-01294-treated and untreated immature, mature and activated gametocytes demonstrated greater than 1.5-fold deregulation of over 359 genes. The majority of these genes are transcriptionally down-regulated in the activated gametocytes and could be assigned to transcription, translation, and signaling indicating a contribution of histone methylations in mediating gametogenesis. Our combined data shows that inhibitors of histone methylation may serve as a multi-stage antimalarials.

2019-11-25 | GSE136008 | GEO

Heart mRNA profiles of TAC 8-weeks wild type (WT) and miR-27b-3p knockout mice

Project description:Aim: The heart undergoes pathological remodelling under increased stress and neuronal imbalance. MicroRNAs (miRNAs) are involved in post-transcriptional regulation of genes in cardiac physiology and pathology. However, the mechanisms underlying miRNA-mediated regulation of pathological cardiac remodelling remain to be studied. This study aims to explore the function of endogenous microRNA-27b-3p (miR-27b-3p) in pathological cardiac remodelling. Methods and results: We found that miR-27b-3p expression was elevated in heart of patients with cardiac hypertrophy and in transverse aortic constriction (TAC)-induced cardiac hypertrophy mouse model. MiR-27b-3p-knockout mice showed significantly attenuated cardiac hypertrophy, fibrosis, and inflammation induced by two independent pathological cardiac hypertrophy models, TAC and Angiotensin II (Ang II) perfusion. Transcriptome sequencing analysis revealed that miR-27b-3p deletion significantly downregulated TAC-induced cardiac hypertrophy, fibrosis, and inflammatory genes. We identified fibroblast growth factor 1 (FGF1) as a novel miR-27b-3p target gene in the heart, which was upregulated in miR-27b-3p-null mice. Conclusions: Our study has demonstrated that miR-27b-3p induces pathological cardiac remodelling and suggests that inhibition of endogenous miR-27b-3p or administration of FGF1 might have the potential to suppress cardiac remodelling in a clinical setting.

2022-07-27 | GSE158191 | GEO

Microarray analysis of heart gene expression in wild type and JMJD2A heart specific transgenic mice after sham and thoracic aortic constriction surgery

Project description:Cardiac hypertrophy and failure are accompanied by a reprogramming of gene expression that involves transcription factors and chromatin remodeling enzymes. Little is known about the role of histone methylation and demethylation in this process. To understand the role of JMJD2A, a trimethyl demethylase for histone 3 lysine 9 and 36, in cardiac hypertrophy, we generated heart specific JMJD2A deletion (JMJD2A hKO) and overexpression (JMJD2A-Tg) mouse lines. JMJD2A hKO and JMJD2A-Tg mice are viable and have no overt baseline phenotype. However, they have altered responses to cardiac stresses. While inactivation of JMJD2A in hKO mice resulted in an attenuated hypertrophic response to transverse aortic constriction (TAC)-induced pressure overload compared to that of control littermates, JMJD2A-Tg mice have exacerbated cardiac hypertrophy after TAC. We identified four-and-a-half LIM domains 1 (FHL1) as a novel target of JMJD2A. JMJD2A binds to the FHL1 promoter in response to TAC and upregulates the expression of FHL1. Binding of JMJD2A to the FHL1 promoter is associated with downregulation of trimethylated H3K9. Upregulation of FHL1 by JMJD2A is mediated through SRF and myocardin, and requires its demethylase activity. The expression of JMJD2A is upregulated in human hypertrophic cardiomyopathy patients. Our studies reveal that JMJD2A promotes cardiac hypertrophy by synergistically upregulating SRF/myocardin-targeted genes and suggest a novel mechanism of reprogramming of gene expression involved in cardiac hypertrophy. Six to eight years old wildtype and JMJD2A heart specific transgnic mice were undergone either sham or TAC surgery. After 3 weeks, mice were sarcirificed to harvest heart. RNA was extracted from heart samples and treated with DNase, followed by biotin-labeling and microarray hybridization.

2011-06-02 | E-GEOD-27689 | biostudies-arrayexpress

Genome-wide analysis of the effect of TUDCA on 1 week transveres aortic constriction (TAC) mouse

Project description:The hypothesis tested in the present study was that ameliorating ER stress by TUDCA could reduce the cardiac remodeling in TAC mice. Results provide important information of the genes that were up- or down-regulated in Veh-TAC operated animals in comparison to Sham, TUDCA -Sham and TUDCA-TAC mice.

2017-04-12 | GSE89539 | GEO

Expression data from murine cardiac fibroblasts and endothelial cells following Transverse Aortic Constriction

Project description:Accumulation of activated cardiac fibroblasts plays a key role in heart failure progression. These cells deposit excessive extracellular matrix that leads to mechanical stiffness, myocyte uncoupling and ischemia. To investigate whether two developmentally distinct cardiac fibroblast populations exhibit distinct expression profiles in response to cardiac injury, and therefore might necessitate distinct therapeutic targeting, we performed microarray analysis on FACS sorted cells. Tie2cre lineage traced CFs, non Tie2cre lineage traced cardiac fibroblasts and endothelial cells were isolated from left ventricle of SHAM operated and banded hearts at the onset of fibrosis, one week after surgery. We used microarrays to detail the global programme of gene expression in cardiac fibroblasts and endothelium following pressure overload. Tie2cre lineage traced, non-tie2cre lineage traced fibroblasts and endothelial cells were sorted from left ventricle of 3 SHAM operated and 3 TAC operated adult male Black Swiss mice. Tie2cre lineage traced, non-tie2cre lineage traced fibroblasts and endothelial cells were sorted from left ventricle of 3 SHAM operated and 3 Transaortic Constriction (TAC) operated adult male Black Swiss mice for RNA extraction and Affymetrix microarray analysis. Hypertrophy in TAC animals, an lack of hypertrophy in SHAM operated animals, was evaluated by hemodynamic measurements before surgery and one week after surgery. Cells were isolated one week after surgery.

2014-05-19 | E-GEOD-45820 | biostudies-arrayexpress

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