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XX chromosome complement promotes, and w-3 fatty acid treatment prevents, adverse statin effects in mice

ABSTRACT: RNA-sequening of livers from male and female C57BL/6J mice fed either chow diet or chow diet + simvastatin (0.1g/kg body weight) for 4 weeks.

ORGANISM(S): Mus musculus

PROVIDER: GSE184588 | GEO | 2024/02/01

REPOSITORIES: GEO

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Sex differences in statin response in hypercholesterolemic (Apoe knockout) Four Core Genotypes mice.

Project description:RNA-sequening of livers from Apoe knockout Four Core Genotypes mice (XX ovaries, XX testes, XY ovaries, XY testes) fed either chow diet or chow diet + simvastatin (0.1g/kg) for 8 weeks.

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Statin induced changes in gene expression in EBV-transformed and native B-cells

Project description:Statin-induced gene expression differences observed in LCLs may be influenced by their transformation, and thus differ from those observed in native B-cells. To assess this possibility, we prepared LCLs and purified B-cells from the same donors, and compared mRNA profiles after 24hr incubation with simvastatin (2M-BM-5M) or sham buffer. We prepared LCLs and purified B-cells from the same donors, and compared mRNA profiles after 24hr incubation with simvastatin (2M-BM-5M) or sham buffer. Genes involved in cholesterol metabolism were similarly regulated between the two cell types under both the statin and sham treated conditions, and the statin-induced changes were significantly correlated.

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Expression data from adult male Sprague Dawley rat liver, investigating how pomegranate skin extract prevents non alcoholic fatty liver diseases

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XX sex chromosome complement promotes atherosclerosis in mice.

Project description: Not available

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Statin induced changes in gene expression in EBV-transformed and native B-cells

2013-11-12 | GSE51444 | GEO

Expression data from adult male Sprague Dawley rat liver, investigating how pomegranate skin extract prevents non alcoholic fatty liver diseases

2016-02-01 | GSE66316 | GEO

Selective mTORC1 inhibition prevents and treats NAFLD and NASH

Project description:We find that selective inhibition of one arm of mTORC1 signaling, via deletion of FLCN, promotes activation of the transcription factor TFE3 and profoundly protects against NAFLD and NASH in mice. (1) We performed genome-wide RNA-seq on livers from Control, liver-specific Flcn-null mice (LiFKO), and Flcn/Tfe3 double knock-out (DKO) mice fed either normal chow (NC) or a NAFLD-inducing diet (AMLN). We find TFE3-mediated induction of lysosomal and mitochondrial gene programs, and also suppression of de novo lipogenesis genes. (2) To understand whether TFE3 directly affects gene expression, we performed TFE3 ChIP-seq on livers from Control and LiFKO mice on normal chow. We find TFE3 occupancy on the chromatin at lysosomal genes, Ppargc1a (a driver of mitochondrial genes), and at de novo lipogenesis genes. (3) Finally, we wanted to test whether TFE3 antagonistically competes with the pro-lipogenic transcription factor SREBP-1c on chromatin. We therefore injected HA-tagged constitutively nuclear (active) SREBP-1c (nSREBP-1c), or a control virus, into control and LiFKO mice, treated them with a NAFLD-inducing diet (FPC diet), and collected liver tissue. We consequently performed HA-nSREBP-1c and TFE3 ChIP-seq experiments and observed no evidence of antagonistic competition.

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