Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA304393 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of whole genome expression changes in livers from wild type animals and animals with a liver specific transgenic over expression of Cyp7a1. Mice were given a chronic, repetitive administration of LPS for 7 days. Our prior analysis had indicated that inflammation suppresses Cyp7a1 and that this leads to accumulation of intermediates in the mevalonate biosynthesis pathway. Here, we hypothesized that over expression of Cyp7a1 would not affect the changes in transcriptional state due to chronic administration of LPS. We provide gene expression data which evaluates this question. Here we find that over expression of Cyp7a1 minimally alters the transcriptome of livers in an untreated state, and that it has small effects on the response to chronic LPS. Total RNA isolated from livers of wild type and liver specific Cyp7a1 transgenic animals treated with or without recurrent, daily LPS injections (1.5mg/kg) for 7 days. There are two biological replicates per condition. Samples are a matrix of all conditions reported as FPKMs.
2016-03-17 | E-GEOD-75477 | biostudies-arrayexpress
Project description:Analysis of whole genome expression changes in livers from wild type animals and animals with a liver specific transgenic over expression of Cyp7a1. Mice were given a chronic, repetitive administration of LPS for 7 days. Our prior analysis had indicated that inflammation suppresses Cyp7a1 and that this leads to accumulation of intermediates in the mevalonate biosynthesis pathway. Here, we hypothesized that over expression of Cyp7a1 would not affect the changes in transcriptional state due to chronic administration of LPS. We provide gene expression data which evaluates this question. Here we find that over expression of Cyp7a1 minimally alters the transcriptome of livers in an untreated state, and that it has small effects on the response to chronic LPS.
2016-03-17 | GSE75477 | GEO
Project description:AID is an intrinsic DNA mutator enzyme and contributes to tumorigenesis through the accumulation of genetic aberrations. To examine whether mutagenesis induced by AID during inflammation-associated hepatocarcinogenesis depends on the transcriptional levels of the target genes, we performed the gene expression profiling of liver tissues from AID transgenic mice and wild-type mice with and without thioacetamide treatment. AID transgenic mice and wild-type mice were administered with thioacetamide in drinking water for 6 months, and the gene expression levels of their livers are compared.
2015-07-10 | E-GEOD-62878 | biostudies-arrayexpress
Project description:Astrocyte mRNA expression - comparison of wild type animals to CETP transgenic animals
| PRJNA436339 | ENA
Project description:To explore the possible changes of gene expression induced by a carcinogen, we treated wild-type and Dicer1-KO mice with one dose of 120 mg/kg N-ethyl-N-nitrosourea (ENU), a model genotoxic carcinogen, and vehicle control. The gene expression profiles were assessed in the mouse livers in wild-type and Dicer1-KO mice design. Total RNA were isolated from the livers at days 15 after the treatment and their expression was determined using Gene Array.
2012-03-06 | GSE36307 | GEO
Project description:Background: Atherosclerosis leads high mortality, highlighting an urgent need for new therapeutic strategies. Protein kinases orchestrate multiple cellular events in atherosclerosis and may provide new therapeutic targets for atherosclerosis. Here, we identified a protein kinase, WEE1 G2 checkpoint kinase (WEE1), promoting inflammatory response in atherosclerosis. Methods: The ApoE-/- mice without macrophage-specific WEE1 deletion (ApoE-/-WEE1f/f) and ApoE-/- mice with macrophage-specific WEE1 deletion (ApoE-/-WEE1MCKO) were generated using bone marrow transplantation. These mice and WEE1 inhibitor MK1775 were used in a high-fat diet (HFD)-induced atherosclerotic model. Human atherosclerotic tissues, mouse primary peritoneal macrophages (MPMs), 293T cells, and recombinant proteins were utilized to investigate the pathogenic role and underlying mechanisms of WEE1. Results: We identified up-regulated p-WEE1 in macrophages in atherosclerotic lesions of HFD-fed ApoE-/- mice. Transcriptome sequencing analysis indicated that WEE1 promotes oxLDL-induced inflammation in macrophages. We then demonstrated that macrophage-specific deletion or pharmacological inhibition of WEE1 attenuates atherosclerosis by reducing inflammation both in vivo and in vitro. The overexpression of wild-type WEE1 or activating-mutant WEE1, but not inactivating-mutant WEE1, exacerbates inflammation in macrophages. Mechanistically, transcriptome sequencing analysis and co-immunoprecipitation followed by quantitative proteomics analysis identified p65 as a binding protein of WEE1. We confirmed that WEE1 directly interacts with the RHD domain of p65 via kinase domain and phosphorylates p65 at S536, thereby facilitating subsequent NF-κB activation and inflammatory response in macrophages. Conclusions: Our findings demonstrated that macrophage WEE1 promotes inflammatory atherosclerosis by directly binding to p65 and phosphorylate it at S536. This study provides WEE1 as a new p65 regulator in inflammation and a potential therapeutic target for atherosclerosis.
2024-03-25 | PXD050932 | Pride
Project description:Serine protease inhibitor Kazal type 3 (Spink3) is a trypsin inhibitor in the pancreas. Spink3-/- pancreatic acinar cells are dead with excessive autophagy at birth (p0.5). To prove the role of nonapoptotic cell death with autophagy, we generated by transgenic technology the pancreas of Spink3-/-;XKI/+ mice contained both normal and dying acinar cells with autophagy. In this new mouse model, chronic inflammation occurred in the pancreas, indicating that some signals from nonapoptotic dead cell induce chronic inflammation in the pancreas. All samples were the pancreas at p0.5. Sample 1 and 2 are the pancreas from wild type (Spink3+/+, control) mice. Sample 3 and 4 are the pancreas from Spink3-/-, which all pancreatic acinar cells show induced nonapoptotic cell death with autophagy. Sample 5 and 6 are the pancreas from Spink3-/-XKI/+, about half acinar cells are normal, but other acinar cells show induced nonapoptotic cell death with autophagy.
2016-07-16 | E-GEOD-48946 | biostudies-arrayexpress
Project description:Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. apolipoprotein E (apoE)-deficient mice, which develop heart failure at an age of 18 months, and non-transgenic C57BL/6J (B6) mice with heart failure triggered by 6 months of pressure overload induced by abdominal aortic constriction (AAC). The development of heart failure was monitored by echocardiography, invasive hemodynamics and histology. The microarray gene expression study of cardiac genes was performed with heart tissue from failing hearts relative to hypertrophic and healthy heart tissue, respectively. The microarray study revealed that the onset of heart failure was accompanied by a strong up-regulation of cardiac lipid metabolism genes involved in fat synthesis, storage and oxidation. Microarray gene expression profiling was performed with heart tissue isolated from (i) 18 month-old apoE-deficient mice relative to age-matched non-transgenic C57BL/6J (B6) mice, (ii) 6 month-old apoE-deficient mice with 2 months of chronic pressure overload induced by abdominal aortic constriction (AAC) relative to sham-operated apoE-deficient mice and nontransgenic B6 mice, (iii) 10 month-old B6 mice with 6 months of AAC relative to sham-operated B6 mice, and (iv) 5 month-old B6 mice with 1 month of AAC relative to age-matched B6 mice.
2010-12-03 | E-GEOD-25765 | biostudies-arrayexpress
Project description:Serum and glucocorticoid-induced kinase 1 (SGK1) regulates blood pressure and has been implicated in inflammation and fibrosis. We have tested whether increased SGK1 activity potentiates mineralocorticoid/NaCl-induced hypertension and kidney injury. To that end we have used a transgenic mouse model with increased SGK1 activity (Tg.sgk1). This data set consists on transcriptomic analysis of kidney cortex samples to obtain differential gene expression due to excess SGK1 activity between wild type or Tg.sgk1 animals that were uninephrectomized and then treated with DOCA/NaCl
2020-08-31 | GSE148880 | GEO
Project description:The aim of the study was to investigate hepatic gene expression profiles differentially regulated by the APOE genotype in gene targeted replacement mice. The APOE4 genotype is associated with increased mortality in the elderly and is an independent risk factor for age-dependent chronic diseases. However, little is known about the underlying mechanisms and molecular targets involved in the APOE4-risk association. As APOE is centrally involved in lipid and cholesterol metabolism and in large part is produced in the liver, we analyzed hepatic RNA profiles of APOE4- and APOE3-expressing mice. 2 groups of 5 animals with 1 liver extract per animal. Mice were homozygous for a human APOE3 or APOE4 gene targeted replacement of the endogenous mouse Apoe gene (B6.129P2-Apoetm2(APOE*3)Mae N8 or B6.129P2-Apoetm3(APOE*4)Mae N8, Taconic Transgenic ModelsM-bM-^DM-", http://www.taconic.com/wmspage.cfm?parm1=2542), purchased at the age of 6-8 weeks, strain C57BL/6, 3 months old at the performance of the microarray, 6 weeks on a high-fat diet containing 41% energy from milk fat and 2 g/kg cholesterol.
2012-12-15 | E-GEOD-42930 | biostudies-arrayexpress