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Data on genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains.

ABSTRACT: The data presented here are related to the research article, entitled Genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains, published in Atherosclerosis 2019 Dec 3;293:1-10 (D. Fuller, A.T. Grainger, A. Manichaikul, W. Shi). The supporting materials include original genotypic and phenotypic data obtained from 266 female F2 mice derived from an intercross between C57BL/6 (B6) and BALB/cJ (BALB) Apoe-/- mice. F2 mice were fed 12 weeks of Western diet, starting at 6 weeks of age. Plasma levels of HDL, LDL cholesterol, triglycerides, glucose and malondialdehyde (MDA) and atherosclerosis in the aortic root and the left carotid artery were measured. 127 microsatellite markers across the entire genome were genotyped. The data is provided in the format ready for QTL analysis with J/qtl and MapManager QTX.

SUBMITTER: Fuller DT

PROVIDER: S-EPMC6997804 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Data on genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains.

Fuller Daniela T DT Grainger Andrew T AT Manichaikul Ani A Shi Weibin W

Data in brief 20200123

The data presented here are related to the research article, entitled Genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains, published in Atherosclerosis 2019 Dec 3;293:1-10 (D. Fuller, A.T. Grainger, A. Manichaikul, W. Shi). The supporting materials include original genotypic and phenotypic data obtained from 266 female F2 mice derived from an intercross between C57BL/6 (B6) and BALB/cJ (BALB) Apoe<sup>-/-</sup> mice. F2 mice ...[more]

PMID: 32025547

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Project description:Purpose: To investigate the diet- or strain-dependence of liver transcriptome in eight Diversity Outbred (DO) founder strains [A/J, C57BL/6J (B6), 129S1/SvImJ (129), NOD/ShiLtJ (NOD), NZO/HILtJ (NZO), and three wild-derived strains CAST/EiJ (CAST), PWK/PhJ (PWK), and WSB/EiJ (WSB)] Methods: Total RNA from eight DO founder strains was extracted from snap frozen liver using Maxwell® 16 LEV simplyRNA Tissue Kit (Promega) according to the manufacturer’s protocol. The quality and amount of liver RNA was evaluated using a qubit RNA assay (Invitrogen R11490) and run on an Biorad Bioanalyzer Chip to verify RNA integrity. RNASeq library was prepared by using Illumina TruSeq RNA library construction protocol. RNA samples from 24 mice-fed AIN-93 M diet and 24 mice-fed HFCA diet were submitted to the David H. Murdock Research Institute (DHMRI) for sequencing. The RNA-seq libraries were constructed from 1 µg total RNA after poly-A library preparation. The pooled libraries were sequenced on two lanes of the Illumina HiSeq2500 Instrument. Results: Our liver transcriptomic analysis of eight mouse strains shows that diet and genetic background have a strong effect on the liver transcriptome, which may be related to differences in cardo-metabolic traits. We calculated a gene module consisting of highly correlated transcripts that enriched the biological pathway and provided a searchable database of liver transcript profiles. To further investigate the association of hepatic gene modules with cardio-metabolic traits, Fmo3, a key enzyme in the production of trimethylamine N-oxide (TMAO), and Nox4, which showed strong association with plasma TMAO and liver triglyceride, were identified as the highest expressed in the laboratory-like inbred strains (B6, 129 and NZO) and the lowest expressed transcripts in the CAST strain. We found differences in the production of TMAO and liver triglyceride, which contributes to metabolic syndrome, depending on genetic backgrounds. Conclusions: Our study provide a valuable data resource to the research community and show that liver transcriptomic analysis identified diet- or strain-specific pathways to pathogenesis of metabolic syndrome.

Project description:Genetic variability in the strength and precision of fear memory is hypothesised to contribute to the etiology of anxiety disorders, including post-traumatic stress disorder. We generated fear-susceptible (F-S) or fear-resistant (F-R) phenotypes from an F8 advanced intercross line (AIL) of C57BL/6J and DBA/2J inbred mice by selective breeding. We identified specific traits underlying individual variability in Pavlovian conditioned fear learning and memory. Offspring of selected lines differed in the acquisition of conditioned fear. Furthermore, F-S mice showed greater cued fear memory and generalised fear in response to a novel context than F-R mice. F-S mice showed greater basal corticosterone levels and hypothalamic corticotrophin-releasing hormone (CRH) mRNA levels than F-R mice, consistent with higher hypothalamic-pituitary-adrenal (HPA) axis drive. Hypothalamic mineralocorticoid receptor and CRH receptor 1 mRNA levels were decreased in F-S mice as compared with F-R mice. Manganese-enhanced magnetic resonance imaging (MEMRI) was used to investigate basal levels of brain activity. MEMRI identified a pattern of increased brain activity in F-S mice that was driven primarily by the hippocampus and amygdala, indicating excessive limbic circuit activity in F-S mice as compared with F-R mice. Thus, selection pressure applied to the AIL population leads to the accumulation of heritable trait-relevant characteristics within each line, whereas non-behaviorally relevant traits remain distributed. Selected lines therefore minimise false-positive associations between behavioral phenotypes and physiology. We demonstrate that intrinsic differences in HPA axis function and limbic excitability contribute to phenotypic differences in the acquisition and consolidation of associative fear memory. Identification of system-wide traits predisposing to variability in fear memory may help in the direction of more targeted and efficacious treatments for fear-related pathology.

Dataset Information

Data on genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains.

Publications

Data on genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains.

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