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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cardiac-specific Bmi1 deletion [mouse]

ABSTRACT: To explore the primary cause of Dilated Cardiomyopathy in Bmi1-null mice, we set out to identify differentially expressed genes by massively parallel sequencing of heart samples from Bmi1f/f;αMHCTM-Cretg/+ mice versus αMHCTM-Cretg/+ control mice (17 weeks postinduction).

ORGANISM(S): Mus musculus

PROVIDER: GSE64391 | GEO | 2015/01/13

SECONDARY ACCESSION(S): PRJNA270875

REPOSITORIES: GEO

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cardiac-specific Bmi1 deletion [mouse]

Project description:To explore the primary cause of Dilated Cardiomyopathy in Bmi1-null mice, we set out to identify differentially expressed genes by massively parallel sequencing of heart samples from Bmi1f/f;?MHCTM-Cretg/+ mice versus ?MHCTM-Cretg/+ control mice (17 weeks postinduction). Methods: Heart mRNA profiles of 17-weeks post-induction Bmi1f/f; MHCTM-Cretg/+ mice and MHCTM-Cretg/+ control mice were generated by deep sequencing, in triplicate, using Illumina GAIIx. Sequence reads were pre-processed with Cutadapt 1.2.1, to remove TruSeq adapters and mapped on the mouse transcriptome (Ensembl gene-build GRCm38.v70) using RSEM v1.2.3. The Bioconductor package EdgeR was used to normalize data with TMM and to test for differential expression of genes using GLM.

2015-01-13 | E-GEOD-64391 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cardiac-specific Bmi1 deletion [human]

Project description:To explore the primary cause of Dilated Cardiomyopathy in heart samples from DCM-diagnosed patients who had undergone heart transplant (hDCM), we set out to identify differentially expressed genes by massively parallel sequencing of heart samples. Methods: Heart mRNA profiles from DCM-diagnosed patients who had undergone heart transplant (hDCM) were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2015-01-30 | E-GEOD-65446 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cardiac-specific Bmi1 deletion [human]

2015-01-30 | GSE65446 | GEO

KDM8 epigenetically controls cardiac metabolism to prevent initiation of dilated cardiomyopathy [CUT&Tag]

Project description:Cardiac metabolism is deranged in heart failure, but underlying mechanisms remain unclear. Lysine demethylase 8 (Kdm8) represses gene expression in the embryo and controls metabolism in cancer. However, its function in cardiac homeostasis is unknown. We show that Kdm8 maintains a mitochondrial gene network active by repressing Tbx15 to prevent dilated cardiomyopathy leading to lethal heart failure. Deletion of Kdm8 in mouse cardiomyocytes increased H3K36me2 with activation of Tbx15 and repression of target genes in the NAD+ pathway before dilated cardiomyopathy initiates. Moreover, NAD+ supplementation prevented dilated cardiomyopathy in Kdm8 mutant mice and TBX15 overexpression blunted NAD+-activated cardiomyocyte respiration. Furthermore, KDM8 was downregulated in human hearts affected by dilated cardiomyopathy and higher TBX15 expression defines a subgroup of affected hearts with the strongest downregulation of genes encoding mitochondrial proteins. Thus, KDM8 represses TBX15 to maintain cardiac metabolism. Our results suggest that epigenetic dysregulation of metabolic gene networks initiates myocardium deterioration towards heart failure and could underlie heterogeneity of dilated cardiomyopathy.

2022-12-23 | GSE215793 | GEO

KDM8 epigenetically controls cardiac metabolism to prevent initiation of dilated cardiomyopathy [RNA-seq]

2022-12-23 | GSE215351 | GEO

Med1 is Necessary for Cardiac Function

Project description:Analysis of ventricular derived mRNA from Med1fl/fl and Med1fl/fl cardiac knockout mice. Results provide insight into the molecual rmechanisms underlying dilated cardiomyopathy.

2017-08-24 | GSE84160 | GEO

Cardiac disruption of SDHAF4-mediated mitochondrial complex II assembly promotes dilated cardiomyopathy

Project description:Succinate dehydrogenase, which is known as mitochondrial complex II, has proven to be a fascinating machinery, attracting renewed and increased interest in its involvement in human diseases. Herein, we find that succinate dehydrogenase assembly factor 4 (SDHAF4) is downregulated in cardiac muscle in response to pathological stresses and in diseased hearts from human patients. Cardiac loss of Sdhaf4 suppresses complex II assembly and results in subunit degradation and complex II deficiency in fetal mice. These defects are exacerbated in young adults with globally impaired metabolic capacity and activation of dynamin-related protein 1, which induces excess mitochondrial fission and mitophagy, thereby causing progressive dilated cardiomyopathy and lethal heart failure in animals. Targeting mitochondria via supplementation with fumarate or inhibiting mitochondrial fission improves mitochondrial dynamics, partially restores cardiac function and prolongs the lifespan of mutant mice. Moreover, the addition of fumarate is found to dramatically improve cardiac function in myocardial infarction mice. These findings reveal a vital role for complex II assembly in the development of dilated cardiomyopathy and provide additional insights into therapeutic interventions for heart diseases.

2022-08-12 | MTBLS4579 | MetaboLights

Elucidation of BMI1, RYBP and H2AK119ub interactomes in Glioblastoma

Project description:Identification of BMI1, RYBP and H2AK119UB interactome in Glioblastoma (GBM) to elucidate BMI1 roles independent of the PRC1-complex in GBM.

2021-09-09 | PXD022057 | Pride

Bmi1 defines long-term adult cardiac stem cells in heart homeostasis and repair

Project description:We have found the existence of a Bmi1+ population in the adult heart contributing to the organ low-rate turnover and repair with the generation of new cardiomyocytes. We show that the Bmi1+ population is a sub-population of the cardiac Sca-1+ progenitor cells. We have analyzed the gene profile by deep-sequencing (RNA-Seq) of Bmi1+ and Sca-1+Bmi1- cells in homeostatic heart condition. On the other hand, we have compared gene profile by deep-sequencing (RNA-Seq) of Bmi1+ cells in homeostatic condition versus Bmi1+ cells 5 days after myocardial infarction (MI). Analysis of RNA-Seq data revealed a differential expression signature between both subsets of cardiac stem/progenitors cells in homeostatic condition and also differences between Bmi1+ cells after AMI versus homeostatic condition.

2017-02-14 | GSE55754 | GEO

Gene expression in the liver of Bmi1 knockout mice

Project description:To explore the potential targets of Bmi1 in the liver development of hepatic carcinogenesis, we assayed the gene expression level in the liver of Bmi1 knockout mice. We isolated the liver tissue of Bmi1 WT and KO mice around 6-8 weeks. Then we extracted total RNA and run the microarray detection. Gene expression in Bmi1 KO mouse livers was compared with that in Bmi1 WT mouse livers to screen potential targets of Bmi1.

2018-03-29 | GSE97170 | GEO

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