Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling

ABSTRACT: Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling

PROVIDER: PRJNA887058 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21802065.fastq.gz	Fastqsanger.gz
	SRR21802066.fastq.gz	Fastqsanger.gz
	SRR21802067.fastq.gz	Fastqsanger.gz
	SRR21802068.fastq.gz	Fastqsanger.gz
	SRR21802069.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling

Project description:The cytochrome P450 reductase (POR) transfers electrons to all microsomal cytochrome P450 enzymes (CYP450) thereby driving their activity. In the vascular system, the POR/CYP450 system has been linked to the production of epoxyeicosatrienoic acids (EETs) but also to the generation of reactive oxygen species. In cardiac myocytes (CMs), EETs have been shown to modulate the cardiac function and have cardioprotective effects. The functional importance of the endothelial POR/CYP450 system in the heart is unclear and was studied here using endothelial cell-specific, inducible knockout mice of POR (ecPOR-/-). RNA sequencing of murine cardiac cells revealed a cell type-specific expression of different CYP450 homologues. Cardiac endothelial cells mainly expressed members of the CYP2 family which produces EETs, and of the CYP4 family that generates omega fatty acids. Tamoxifen-induced endothelial deletion of POR in mice led to cardiac remodelling under basal conditions, as shown by an increase in heart weight to body weight ratio and an increased CM area as compared to control animals. Endothelial deletion of POR was associated with a significant increase in endothelial genes linked to protein synthesis with no changes in genes of the oxidative stress response. CM of ecPOR-/- mice exhibited attenuated expression of genes linked to mitochondrial function and an increase in genes related to cardiac myocyte contractility. In a model of pressure overload (transverse aortic constriction, TAC with O-rings), ecPOR-/- mice exhibited an accelerated reduction in cardiac output (CO) and stroke volume (SV) as compared to control mice. These results suggest that loss of endothelial POR along with a reduction in EETs leads to an increase in vascular stiffness and loss in cardioprotection, resulting in cardiac remodelling.

2022-12-21 | GSE214776 | GEO

Proteomic Consequences of the Deletion of Cytochrome P450 (CYP450) Reductase in Mice

Project description:Microsomal cytochrome P450 (CYP450) reductase enzymes play a major role in drug and xenobiotic metabolism. Mice which are deficient in hepatic CYP450 reductase serve as excellent models in understanding CYP450 drug metabolism and alterations in the underlying biology. A reversed-phase nano-bore UPLC-MS-based proteomic analysis, using an untargeted data independent approach (DIA), has been utilized for liver tissue extracts to evaluate differences between the proteomes of wild type (C57Bl6) and hepatic P450 reductase mice (HRNTM). Statistically curated, differential expressed protein groups highlighted a variety of molecular and biological functions, including binding and catalytic related activities. Pathway enrichment analysis resulted in perturbation of lipid and energy related pathways, which included bile acid biosynthesis, fatty acid omega oxidation and tricarbonic acid (TCA) cycle as examples.

2022-05-26 | PXD024420 | Pride

Transcription profiling of mouse models with liver-specific deletion or global hypomorphic expression of the NADPH-cytochrome P450 reductase gene to study molecular mechanisms for the regulation of microsomal cytochrome P450 and the fatty liver phenotype.

Project description:NADPH-cytochrome P450 reductase (CPR) is important for the functions of many enzymes, such as microsomal cytochrome P450 (P450) monooxygenases and heme oxygenases. Two mouse models with deficient CPR expression in adults were recently generated in this laboratory: liver-Cpr-null (with liver-specific Cpr deletion) (Gu et al., J. Biol. Chem., 278, 25895-25901, 2003) and Cpr-low (with reduced CPR expression in all organs examined) (Wu et al. J. Pharmacol. Expt. Ther. 312, 35-43, 2005). The phenotypes included a reduced serum cholesterol level and an induction of hepatic P450 in both models, and hepatomegaly and fatty liver in the liver-Cpr-null mouse alone. Our aim was to identify hepatic gene-expression changes related to these phenotypes. Cpr-lox mice, which have normal CPR expression (Wu et al., Genesis, 36, 177-181, 2003.), were used as the control in microarray analysis. A detailed analysis of the gene-expression changes in lipid metabolism and transport pathways revealed potential mechanisms, such as an increased activation of constitutive androstane receptor (CAR) and a decreased activation of peroxisomal proliferators activated receptor alpha (PPARï?¡) by precursors of cholesterol biosynthesis, that underlie common changes (e.g., induction of multiple P450s and inhibition of genes for fatty acids metabolism) in response to CPR-loss in the two mouse models. Moreover, we also uncovered model-specific gene-expression changes, such as the induction of a lipid translocase (CD36 antigen) and the suppression of carnitine O-palmitoyltransferase 1 (CPT1a) and acyl-CoA synthetase long-chain family member 1 (Acsl1), that are potentially responsible for the severe hepatic lipidosis observed in liver-Cpr-null, but not Cpr-low mice.

2007-08-31 | E-GEOD-2362 | biostudies-arrayexpress

Hepatic reductase null

Project description:Microarray analysis to examine the relationship between hepatic phenotype and changes in gene expression in cytochrome P450 reductase (CPR) null mice. Keywords: ordered

2004-07-11 | GSE1468 | GEO

Endothelial deletion of the cytochrome P450 reductase leads to cardiac remodelling.

| S-EPMC9755668 | biostudies-literature

Transcription profiling of mouse P458 reductase (CPR) animals

Project description:Microarray analysis to examine the relationship between hepatic phenotype and changes in gene expression in cytochrome P450 reductase (CPR) null mice.

2008-06-11 | E-GEOD-1468 | biostudies-arrayexpress

Identification and developmental expression of the full complement of cytochrome P450 genes in zebrafish

Project description:To determine the expression of cytochrome P450 genes during normal development

2010-10-21 | GSE24840 | GEO

Identification and developmental expression of the full complement of cytochrome P450 genes in zebrafish

Project description:To determine the expression of cytochrome P450 genes during normal development Zebrafish embryos were collected at 3, 6, 12, 24, 36, and 48 hours post fertilization. Quadruplicate biological replicates of 100 embryos were hybridized.

2010-10-21 | E-GEOD-24840 | biostudies-arrayexpress

RNA-seq profiling of Pleurotus ostreatus exposed to BBP with or without cytochrome P450 inhibition

Project description:This study provides transcriptomic insights into the degradation of butyl benzyl phthalate (BBP) by the white-rot fungus Pleurotus ostreatus. RNA-seq was conducted for samples treated with BBP alone or in combination with the cytochrome P450 inhibitor piperonyl butoxide (PB). The aim was to investigate the role of fungal enzymes in BBP metabolism. Differentially expressed genes related to xenobiotic degradation, oxidative stress, and P450 activity were identified and analyzed.

2025-08-01 | GSE302615 | GEO

Fetal to adult ontogeny of human cytochrome P450 activity, abundance, and expression

Project description:Activity-based and global proteomic analysis of fetal through late adulthood human samples, with a primary focus on cytochrome P450 enzyme expression and functional activity

2018-10-24 | PXD002781 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data