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RNA-seq of hepatic mRNA from 21 week old PAI-1 +/- and littermate control mice fed standard chow

ABSTRACT: RNA-seq of hepatic mRNA from 21 week old PAI-1 +/- and littermate control mice fed standard chow

PROVIDER: PRJNA636505 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11905204.fastq.gz	Fastqsanger.gz
	SRR11905205.fastq.gz	Fastqsanger.gz
	SRR11905206.fastq.gz	Fastqsanger.gz
	SRR11905207.fastq.gz	Fastqsanger.gz
	SRR11905208.fastq.gz	Fastqsanger.gz

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RNA-seq of hepatic mRNA from 21 week old PAI-1 +/- and littermate control mice fed standard chow

Project description:We report RNA-seq data from hepatic mRNA on WT and PAI-1 heterozygous 21 week old mice.

2020-11-01 | GSE151597 | GEO

RNA-seq of hepatic mRNA in mice fed chow with and without the PAI-1 inhibitor TM5614

Project description:We report RNA-seq data from hepatic mRNA in mice on standard chow. Mice 41-45 were fed standard chow. Mice 46-50 were fed standard chow + a PAI-1 inhibitor, TM5614 for 10 days.

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Gene expression profile at single cell level of islets from two β-cell specific knockout mouse models (βZKO-Mip and βZKO-Rip), littermate controls (Zzef1f/f), and the MIP-Cre mice fed with normal-chow diet (NCD).

Project description:Islet consists of multiple cell types that work in concert to orchestrate their endocrine function. To rule out of direct effect of diet or phenotype, we performed comparative single-cell RNA-sequencing (scRNA-seq) on 12-week βZKO-Mip, βZKO-Rip mice, littermate controls (Zzef1f/f) and MIP-Cre mice islets fed with normal-chow diet (NCD) by Chromium Next GEM Single Cell 3’ Reagent Kits.

2025-09-22 | GSE273688 | GEO

Gene expression data of islets from Zzef1 global knockout (Zzef1_KO) mice and littermate controls (WT) mice fed with normal-chow diet (NCD) [bulk RNA-seq]

Project description:To understand the global molecular basis of the phenotype caused by the loss of Zzef1 in islets, we isolated pancreatic islets from 12-week-old Zzef1KO and WT mice fed with normal-chow diet (NCD). Then mice were sacrificed and total RNAs were isoloated from islets. We included at least 3-4 independent biological replicates, each composed of RNA isolated from islets of 5 animals with the same genotype. We then performed gene expression profiling analysis using data obtained from islets RNA-seq of Zzef1KO mice and littermates fed a normal chow diet.

2025-09-22 | GSE223143 | GEO

RNA-seq of hepatic mRNA in mice fed chow with and without the PAI-1 inhibitor TM5614

Project description:RNA-seq of hepatic mRNA in mice fed chow with and without the PAI-1 inhibitor TM5614

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Effect of deleting PexRAP/ADHAPR in adipose tissue of chow-fed male C57/BL6J mice

Project description:To investigate the role of PexRAP/ADHAPR in adipose tissue, we use adiponectin-driven Cre recombinase to delete Dhrs7b, the gene which encodes PexRAP/ADHAPR, from all adipose depots. This study assays gene expression in subcutaneous adipose tissue (iWAT) of 8 week old chow-fed male mice.

2023-03-28 | GSE227912 | GEO

Haloperidol and rimonabant increase delay discounting in rats fed high-fat and standard-chow diets.

Project description:The dopamine and endocannabinoid neurotransmitter systems have been implicated in delay discounting, a measure of impulsive choice, and obesity. The current study was designed to determine the extent to which haloperidol and rimonabant affected delay discounting in rats fed standard-chow and high-fat diets. Sprague-Dawley rats were allowed to free-feed under a high-fat diet (4.73 kcal/g) or a standard-chow diet (3.0 kcal/g) for 3 months. Then, operant sessions began in which rats (n=9 standard chow; n=10 high-fat) chose between one sucrose pellet delivered immediately versus three sucrose pellets after a series of delays. In another condition, carrot-flavored pellets replaced sucrose pellets. After behavior stabilized, acute injections of rimonabant (0.3-10 mg/kg) and haloperidol (0.003-0.1 mg/kg) were administered intraperitoneally before some choice sessions under both pellet conditions. Haloperidol and rimonabant increased discounting in both groups of rats by decreasing percent choice for the larger reinforcer and area-under-the-curve values. Rats in the high-fat diet condition showed increased sensitivity to haloperidol compared with chow-fed controls; haloperidol increased discounting in both dietary groups in the sucrose condition, but only in the high-fat-fed rats in the carrot-pellet condition. These findings indicate that blocking dopamine-2 and cannabinoid-1 receptors results in increased delay discounting, and that a high-fat diet may alter sensitivity to dopaminergic compounds using the delay-discounting task.

| S-EPMC4772744 | biostudies-literature

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Project description:Gene expression in livers of male wild-type (WT) and OGG1-deficient (Ogg1-/-) mice fed either a chow diet or a high-fat diet (HFD) were examined. Mice were fed the diet for 10 weeks prior to tissue collection and were 22 weeks of age at the time of tissue collection. 24 Total samples were analyzed. We generated the following pairwise comparisons using GeneSifter: WT Chow vs Ogg1-/- Chow; WT HFD vs. Ogg1-/- HFD using t-test followed by Benjamini and Hochberg correction. An adjusted p-value less than 0.05 was considered to be statistically significant.

2012-12-16 | E-GEOD-35497 | biostudies-arrayexpress

PAI-1 Interaction with Sortilin Related Receptor-1 is Required for Lung Fibrosis

Project description:Plasminogen activator inhibitor-1 (PAI-1) has been previously shown to promote lung fibrosis via a mechanism that requires an intact vitronectin (VTN) binding function. However, in the present study, employing two distinct murine fibrosis models, we show that VTN is not required for PAI-1 to drive lung scarring. This finding suggested that there may be previously unrecognized PAI-1-protein interactions involving the VTN-binding site on PAI-1 and led us to seek novel PAI-1 binding partners that promote fibrosis. Using an unbiased proteomic approach, we identified sortilin related receptor 1 (SorlA) as the most highly enriched PAI-1 interactor in the injured lung. SorlA is a mosaic receptor implicated in cardiovascular disease and Alzheimer’s dementia, but a role for SorlA in lung fibrosis has not been previously described. In the present study, we found that SorlA deficient mice are protected against the development of lung scarring following injury while SorlA heterozygous mice have an intermediate phenotype. We further determined that the SorlA binding site on PAI-1 overlaps with its VTN-binding site and that mutation of amino acid residues required for VTN-binding also reduce PAI-1 binding to SorlA. We further show that, while VTN deficiency does not influence fibrogenesis in the presence or absence of PAI-1, SorlA is required for PAI-1 to promote scarring. These results, together with data showing increased SorlA levels in human IPF lung tissue, support a novel mechanism through which the potent profibrotic mediator PAI-1 drives lung fibrosis and implicate SorlA as a new therapeutic target in IPF treatment

2025-07-14 | PXD054196 | Pride

Gastrin, PAI-1 and mucosal growth. Whole organism studies in transgenic mice.

Project description:We are studying the role of PAI-1 in hypergastrinemic transgenic mice (PAI-1 knockout, HK-ATPase beta knockout and corresponding control strains). As a model of hypergastrinaemia, HK-ATPase beta knockout mice are preferred instead of giving a high dose of proton pump inhibitors daily. We have successfully crossed these two strains and generated double knockout mice (PAI-1--/HK-ATPase--) and 3 different control groups (PAI-1++/HK-ATPase++, PAI-1--/HK-ATPase++ and PAI-1++/HK-ATPase--) (9 animals in each group). The gastric phenotype of all mice has been examined by morphologic and molecular analysis after 12 months. Gastric biopsies and blood samples have been taken for histology, large scale gene expression analysis, verification of mRNA and protein expression and gastrin measurements. Global gene expression analysis has been done on gastric mucosal samples from all groups of mice. The differences between wild type mice and the transgenic animals are expected to provide novel hypotheses on the role of PAI-1 in gastrin-induced changes in the gastric mucosa.

2016-02-01 | E-MTAB-3853 | biostudies-arrayexpress

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