CYP2J2 Modulates Diverse Transcriptional Programs in Adult Human Cardiomyocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA564110 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10074824_1.fastq.gz | Fastqsanger.gz | |||
| SRR10074824_2.fastq.gz | Fastqsanger.gz | |||
| SRR10074825_1.fastq.gz | Fastqsanger.gz | |||
| SRR10074825_2.fastq.gz | Fastqsanger.gz | |||
| SRR10074826_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:CYP2J2, a member of the Cytochrome P450 family of enzymes, is the most abundant epoxygenase in the heart and has multifunctional properties including bioactivation of epoxyeicosatrienoic acids, which, in turn, have been implicated in mediating several cardiovascular conditions. In order to elucidate the complex role played by CYP2J2 in cardiac tissue, we performed targeted silencing of CYP2J2 expression in human adult cardiomyoctes and interrogated whole genome transcriptional responses. We found that knockdown of CYP2J2 elicits widespread alterations in gene expression of ventricular cardiomyocytes and leads to the activation of a diverse repertoire of programs, including those involved in ion channel signaling, development, extracellular matrix, and metabolism. Several members of the differentially up-regulated ion channel module have well-known pathogenetic roles in cardiac dysrhythmias. By leveraging causal network and upstream regulator analysis, we identified several candidate drivers of the observed transcriptional response to CYP2J2 silencing; these master regulators have been implicated in aberrant cardiac remodeling, heart failure, and myocyte injury and repair. Collectively, our study demonstrates that CYP2J2 plays a central and multifaceted role in cardiomyocyte homeostasis, and provides a framework for identifying critical regulators and pathways influenced by this gene.
2020-03-07 | GSE136957 | GEO
Project description:CYP2J2, a member of the Cytochrome P450 family of enzymes, is the most abundant epoxygenase in the heart and has multifunctional properties including bioactivation of arachidonic acid to epoxyeicosatrienoic acids, which, in turn, have been implicated in mediating several cardiovascular conditions. Using a proteomic approach, we found that CYP2J2 expression is lower in cardiac tissue from patients with cardiomyopathy compared to controls. In order to better elucidate the complex role played by CYP2J2 in cardiac cells, we performed targeted silencing of CYP2J2 expression in human adult ventricular cardiomyocytes and interrogated whole genome transcriptional responses. We found that knockdown of CYP2J2 elicits widespread alterations in gene expression of ventricular cardiomyocytes and leads to the activation of a diverse repertoire of programs, including those involved in ion channel signaling, development, extracellular matrix, and metabolism. Several members of the differentially up-regulated ion channel module have well-known pathogenetic roles in cardiac dysrhythmias. By leveraging causal network and upstream regulator analysis, we identified several candidate drivers of the observed transcriptional response to CYP2J2 silencing; these master regulators have been implicated in aberrant cardiac remodeling, heart failure, and myocyte injury and repair. Collectively, our study demonstrates that CYP2J2 plays a central and multifaceted role in cardiomyocyte homeostasis and provides a framework for identifying critical regulators and pathways influenced by this gene in cardiovascular health and disease.
| S-EPMC7093536 | biostudies-literature
Project description:Adult ventricular cardiomyocytes
| PRJNA556434 | ENA
Project description:Expression profiles of microRNAs in neonatal (isolated from day0 newborn rats) and adult rat cardiomyocytes (isolated from 2month old rats) Two condition experiment; Biological replicates: 7 samples of cardiomyocytes from neonatal rats (from independent isolations); 6 samples of cardiomyocytes isolated from adult animals (from independent isolations)
2012-10-13 | E-GEOD-41537 | biostudies-arrayexpress
Project description:ChIP assay in adult ventricular cardiomyocytes
| PRJNA556435 | ENA
Project description:We addressed the question of which protein kinases are expressed in cardiomyocytes. We assessed the changes during postnatal development, comparing profiles in rat neonatal ventricular cardiomyocytes (NVMs) with adult ventricular cardiomyocytes (AVMs). Neonatal and adult rat ventricular cardiomyocytes prepared according to established procedures (Marshall et al. PLoS ONE 2010 5(4):e10027; Fuller and Sugden, FEBs Lett. 1989 247:209-12; Rodrigues and Severson In Biochemical Techniques in the Heart (McNeill, J. H., Ed.) pp 101-115, CRC Press, New York.). mRNA expression profiles compared using Affymetrix rat genome 230 2.0 arrays.
2015-01-01 | E-MTAB-2832 | biostudies-arrayexpress
Project description:In cardiomyocytes, Ca2+ influx through L-type voltage-gated calcium channels (LTCCs) following membrane depolarization regulates crucial Ca2+-dependent processes including duration and amplitude of the action potentials and excitation-contraction coupling. LTCCs are heteromultimeric proteins composed of the Cav1, Cav, Cav2 and Cav subunits. Here, using ascorbate peroxidase (APEX)-mediated proximity labeling and quantitative proteomics, we identified 61 proteins in the nano-environments of Cav2 in cardiomyocytes. These proteins are involved in diverse cellular functions such as cellular trafficking, muscular contraction, sarcomere organization and excitation-contraction coupling. Moreover, pull-down assays, co-immunoprecipitation analyses and super-resolution imaging using direct stochastic optical reconstruction microscopy (dSTORM) revealed that Cav2 interacts with the ryanodine receptor 2 (RyR2) in adult cardiomyocytes, probably coupling LTCCs and the RyR2 into a supramolecular complex at the dyads. This interaction is mediated by the Src-homology 3 domain of Cav2 and is necessary for an effective pacing frequency‐dependent increase of the Ca2+-induced Ca2+ release mechanism in cardiomyocytes.
2021-12-14 | PXD021375 | Pride
Project description:Genome-wide gene expression analysis at different stages of cardiomyocyte differentiation (undifferentiated mouse embryonic stem cells, neonatal mouse cardiomyocytes and adult mouse cardiomyocytes). Results provide important information on the differential expressed genes between undifferentiated mouse embrionic stem cells (mES) and mouse cardiomyocytes (CM) and also between cardiomyocytes from neonatal (CMp) and adult stages (CMa). This dataset allowed us to compare the expression profile of mES, CMp and CMa with the epigenetic profile of histone methylation generated with ChIP-seq experiments. Total RNA was obtained from biological triplicate of undifferentiated mouse embryonic stem cells (mES), neonatal mouse cardiomyocytes (CMp) and adult mouse cardiomyocytes (CMa)
2014-12-22 | E-GEOD-44829 | biostudies-arrayexpress
Project description:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. We have identified fractalkine as a possible novel mediator in HF development. To address this issue, we have performed microarray analysis of cardiomyocytes treated with different isoforms of fractalkine. Methods: Cardiomyocytes isolated from adult rat hearts and treated with different forms of fractalkine for 24 hours. Control cells were treated with BSA. Molecular alterations in myocardial tissue were measured by using cDNA microarrays. Molecular pathways affected were identified by the Ingenuity Pathway Analysis software. Results: Several molecular pathways were affected upon fractalkine stimulation of adult cardiomyocytes. Keywords: Fractalkines effect on cardiomyocytes
2008-02-01 | GSE7397 | GEO
Project description:PRO-seq assay in adult ventricular cardiomyocytes
| PRJNA556436 | ENA