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Transcriptomics Analysis of bulk RNA from dissected brain regions (medial prefrontal cortex, cerebellum, and hippocampus) from 129/Sv-Cyp2e1tm1Gonz/J (CYP2E1-KO) and 129S1/SvImJ (WT) mice

ABSTRACT: To establish the consequences of whole-animal deletion of CYP2E1, we isolated RNA from dissected brain tissue (cerebellum, medial prefrontal cortex, dorsal hippocampus, and ventral hippocampus) of 16-week male and female WT and KO mice. Mice were maintained on a normal chow diet and were euthanized using CO2 and decapitation prior to brain dissection.

ORGANISM(S): Mus musculus

PROVIDER: GSE307546 | GEO | 2025/12/31

REPOSITORIES: GEO

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Total RNA-seq using mouse tissues from Cyp2e1 +/+ mice upon pair-fed, Cyp2e1 +/+ mice upon EtOH-fed, Cyp2e1 -/- mice upon pair-fed, and Cyp2e1 -/- mice upon EtOH fed.

Project description:To investigate the effect of Cyp2e1 and EtOH on mRNA expression in mouse tissues, we profiled total RNA expression using mouse tissues from Cyp2e1 -/- mice and Cyp2e1 +/+ mice upon EtOH fed mice compared to control. We compare the expression level of RNA and profile circular RNA expression using circular RNA junction.

2024-06-30 | GSE206348 | GEO

NOD x 129.H2(g7) backcross delineates 129S1/SvImJ-derived genomic regions modulating type 1 diabetes development in mice.

Project description:ObjectiveIntroduction of genes targeted in 129/Sv embryonic stem (ES) cells into NOD mice brings about linked genes that may modulate type 1 diabetes. Our objective was to identify 129S1/SvJ non-MHC regions contributing type 1 diabetes resistance or susceptibility in backcross to NOD/LtJ.Research design and methodsAfter congenic transfer of the NOD H2(g7) haplotype onto 129S1/Sv, 310 females were produced by NOD x (NOD x 129.H2(g7))F1 backcross (N2). A genome scan for quantitative trait locus (QTL) affecting clinical diabetes, age of diabetes onset, and insulitis severity was performed using subphenotype characteristics to improve power and resolution for detection of diabetes susceptibility loci.ResultsThirty-six of 310 (11.6%) N2 females developed type 1 diabetes between 14 and 40 weeks. Significant evidence of linkage for only a single previously reported Idd complex locus (Idd10/17/18, chromosome [Chr] 3) was indicated for clinical diabetes. The quantitative traits of insulitis either alone or combined with age at type 1 diabetes onset were significantly linked to known Idd regions on Chr 1 (Idd5 region), Chr 4 (Idd9 region), Chr 8 (Idd22), Chr 11 (Idd4.3), and proximal Chr 17 (Idd16 region). Significant 129S1/Sv resistance contributions were identified on Chr 1, 15 (two loci), and 19, with suggestive evidence for additional novel 129/Sv resistance QTL on Chr 5 and 17 and susceptibility on Chr 2.ConclusionsThe 129S1/SvJ genome harbors collections of both known and potentially novel non-MHC Idd loci. Investigators targeting 129/Sv genes mapping within chromosomal regions reported herein or elsewhere in the genome need to exclude potential contributions from linked Idd loci by generating a NOD.129 control strain expressing the nontargeted allele.

| S-EPMC2699846 | biostudies-literature

Q11, a CYP2E1 inhibitor, exerts anti-hepatocellular carcinoma effect by inhibiting M2 macrophage polarization

Project description:Despite significant advancements in cancer immunotherapy, many patients continue to respond poorly. Novel therapeutic strategies and drugs are urgently needed. Here, we found that CYP2E1 is significantly upregulated in M2 macrophages. The CYP2E1 inhibitor, Q11, could inhibit M2 macrophage polarization, while CYP2E1 overexpression could promote it. Increased levels of CYP2E1 and M2 macrophages in the tumor microenvironment of HCC patients correlate with poor prognosis. Q11 could inhibit tumor cells by targeting M2 macrophages rather than directly attacking tumor cells. Both Q11 and Cyp2e1 knockout could effectively suppress tumor growth. Q11 reduces the production of CYP2E1 metabolites (±)9(10)-DiHOME and (±)12(13)-DiHOME, thus attenuating PPARγ activation and M2 macrophage polarization. In summary, our findings suggest that Q11 could suppress M2 macrophage polarization by modulating the CYP2E1/(±)9(10)-DiHOME or (±)12(13)-DiHOME/PPARγ axis, indicating that CYP2E1 inhibition may be a novel therapeutic strategy for HCC and positioning Q11 as a promising therapeutic agent.

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Total RNA-seq using mouse tissues from Cyp2e1 +/+ mice upon pair-fed, Cyp2e1 +/+ mice upon EtOH-fed, Cyp2e1 -/- mice upon pair-fed, and Cyp2e1 -/- mice upon EtOH fed.

Project description:Total RNA-seq using mouse tissues from Cyp2e1 +/+ mice upon pair-fed, Cyp2e1 +/+ mice upon EtOH-fed, Cyp2e1 -/- mice upon pair-fed, and Cyp2e1 -/- mice upon EtOH fed.

| PRJNA850373 | ENA

Candidate genes for obesity revealed from a C57BL/6J x 129S1/SvImJ intercross.

Project description:ObjectiveTo identify the genes controlling body fat, we carried out a quantitative trait locus (QTL) analysis using C57BL/6J (B6) and 129S1/SvImJ (129) mice, which differ in obesity susceptibility after consuming an atherogenic diet.MethodsMice were fed chow until 8 weeks and an atherogenic diet from 8 to 16 weeks; body fatness was measured by X-ray absorptiometry in 528 (B6 x 129) F(2) at 8 and 16 weeks. A high-density genome scan was performed using 508 polymorphic markers. After identifying the genetic loci, we narrowed the QTL using comparative genomics and bioinformatics.ResultsThe percentage of body fat was significantly linked to loci on chromosomes (Chr) 1 (22, 68 and 173 Mb), 4 (74 Mb), 5 (73 Mb), 7 (88 Mb), 8 (43 and 80 Mb), 9 (55 Mb), 11 (115 Mb) and 12 (32 Mb); three suggestive loci on Chrs 6 (76 Mb), 9 (30 Mb) and 16 (26 Mb) and two pairs of interacting loci (Chr 2 at 99.8 Mb with Chr 7; Chr 1 at 68 Mb with Chr 11). Comparative genomics narrowed the QTL intervals by 20-57% depending on the chromosome; in most cases, haplotype analysis further narrowed them by about 90%.ConclusionsOur analysis identified 15 QTL for percentage of body fat. We narrowed the QTL using comparative genomics and haplotype analysis and suggest several candidate genes: Apcs on Chr 1, Ppargc1a on Chr 5, Ucp1 on Chr 8, Angptl6 on Chr 9 and Lpin1 on Chr 12.

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Deficits across multiple behavioral domains align with susceptibility to stress in 129S1/SvImJ mice.

Project description:Acute physical or psychological stress can elicit adaptive behaviors that allow an organism maintain homeostasis. However, intense and/or prolonged stressors often have the opposite effect, resulting in maladaptive behaviors and curbing goal-directed action; in the extreme, this may contribute to the development of psychiatric conditions like generalized anxiety disorder, major depressive disorder, or post-traumatic stress disorder. While treatment of these disorders generally focuses on reducing reactivity to potentially threatening stimuli, there are in fact impairments across multiple domains including valence, arousal, and cognition. Here, we use the genetically stress-susceptible 129S1 mouse strain to explore the effects of stress across multiple domains. We find that 129S1 mice exhibit a potentiated neuroendocrine response across many environments and paradigms, and that this is associated with reduced exploration, neophobia, decreased novelty- and reward-seeking, and spatial learning and memory impairments. Taken together, our results suggest that the 129S1 strain may provide a useful model for elucidating mechanisms underlying myriad aspects of stress-linked psychiatric disorders as well as potential treatments that may ameliorate symptoms.

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Project description:We report the discrepancy of hepatic mRNA expression in Cyp2e1 widetype and knockout mice by application of RNA-seq technology.

2022-06-01 | GSE193796 | GEO

CYP2E1 TB study

Project description:CYP2E1 gene sequencing data for the drug-susceptible TB study sample set (n = 34)

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Transcriptome profiling of normal and CYP2E1 knockdown human neural progenitor cells

Project description:The objective of the study was to examine changes in gene expression induced by CYP2E1 knockdown in neural progenitor cells.There were 6samples in total.Samples shs_1, shs_2, and shs_3 are the control group, and shCYP2E1_1, shCYP2E1_2, and shCYP2E1_3 are the CYP2E1 knockdown group.Neural progenitor cells were cultured in vitro from normal fetal brain tissue aborted at 21 weeks, infected with CYP2E1_shRNAs and CYP2E1_shRNA lentivirus respectively, and then differentiated and cultured for 4 days.The total RNA of each sample was extracted from the lentivirus infected, early differentiated human neural progenitor cells with TRIzol reagent.Then the RNA samples were processed for high throughput transcriptome sequencing on Illumina HiSeq 3000 platform.

2025-08-31 | GSE278691 | GEO

Quantitative trait loci for sensitivity to ethanol intoxication in a C57BL/6J×129S1/SvImJ inbred mouse cross.

Project description:Individual variation in sensitivity to acute ethanol (EtOH) challenge is associated with alcohol drinking and is a predictor of alcohol abuse. Previous studies have shown that the C57BL/6J (B6) and 129S1/SvImJ (S1) inbred mouse strains differ in responses on certain measures of acute EtOH intoxication. To gain insight into genetic factors contributing to these differences, we performed quantitative trait locus (QTL) analysis of measures of EtOH-induced ataxia (accelerating rotarod), hypothermia, and loss of righting reflex (LORR) duration in a B6×S1 F2 population. We confirmed that S1 showed greater EtOH-induced hypothermia (specifically at a high dose) and longer LORR compared to B6. QTL analysis revealed several additive and interacting loci for various phenotypes, as well as examples of genotype interactions with sex. QTLs for different EtOH phenotypes were largely non-overlapping, suggesting separable genetic influences on these behaviors. The most compelling main-effect QTLs were for hypothermia on chromosome 16 and for LORR on chromosomes 4 and 6. Several QTLs overlapped with loci repeatedly linked to EtOH drinking in previous mouse studies. The architecture of the traits we examined was complex but clearly amenable to dissection in future studies. Using integrative genomics strategies, plausible functional and positional candidates may be found. Uncovering candidate genes associated with variation in these phenotypes in this population could ultimately shed light on genetic factors underlying sensitivity to EtOH intoxication and risk for alcoholism in humans.

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