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Attenuation of early atherogenesis in LDLR-KO mice by proteasome inhibition

ABSTRACT: To get further insights into the processes leading to attenuation of early stage atherosclerosis in the bortezomib treated LDLR-KO mice, microarray profiling of gene expression was performed on RNA taken from whole aortae of bortezomib treated LDLR-KO and sham- treated LDLR-KO mice fed a Western diet for 6 weeks and compared the changes in gene expression in both groups to non-atherosclerotic CD animals. Male 10-week-old LDLR-KO mice (B6.129S7-Ldlrtm1Her/J; JAX Mice, Boston) were fed a Western-type diet for 6 weeks ad libitum and received intraperitoneal injections of bortezomib (50 µg/kg body weight; WD+Bor) or saline (WD) twice weekly (n = 4). Mice that were fed normal diet served as chow diet control (CD; n = 4). Gene expression in aortic tissue was measured. Two independent experiments were performed.

ORGANISM(S): Mus musculus

SUBMITTER: Antje Ludwig

PROVIDER: E-GEOD-30638 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Attenuation of early atherogenesis in LDLR-KO mice by proteasome inhibition

Project description:To get further insights into the processes leading to attenuation of early stage atherosclerosis in the bortezomib treated LDLR-KO mice, microarray profiling of gene expression was performed on RNA taken from whole aortae of bortezomib treated LDLR-KO and sham- treated LDLR-KO mice fed a Western diet for 6 weeks and compared the changes in gene expression in both groups to non-atherosclerotic CD animals.

2011-07-14 | GSE30638 | GEO

Liver proteiomic analysis on westeren diet fed mice under oral supplementation of indole-3-acetate

Project description:Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries. There is growing evidence that dysbiosis of the intestinal microbiota and disruption of microbiota-host interactions contribute to the pathology of NAFLD. We previously demonstrated that gut microbiota derived tryptophan metabolite indole-3-acetate (I3A) was decreased in both cecum and liver of high-fat diet-fed mice and attenuated the expression of inflammatory cytokines in macrophages and TNF-a and fatty acid induced inflammatory responses in an aryl-hydrocarbon receptor (AhR) dependent manner in hepatocytes. In this study, we investigated the effect of orally administered I3A in a mouse model of diet induced NAFLD. Western diet (WD)-fed mice given sugar water (SW) with I3A showed dramatically decreased serum ALT, hepatic TG, liver steatosis, hepatocyte ballooning, lobular inflammation, and hepatic production of inflammatory cytokines, compared to WD-fed mice given only SW. Metagenomic analysis show that I3A administration did not significantly modify the intestinal microbiome, suggesting that I3A’s beneficial effects likely reflect the metabolite’s direct actions on the liver. Administration of I3A partially reversed WD induced alterations of liver metabolome and proteome, notably, decreasing expression of several enzymes in hepatic lipogenesis and β- oxidation. Mechanistically, we also show that AMP-activated protein kinase (AMPK) mediates the anti-inflammatory effects of I3A in macrophages. The potency of I3A in alleviating liver steatosis and inflammation clearly demonstrates its potential as a therapeutic modality for preventing the progression of steatosis to NASH.

2024-02-23 | PXD046255 | Pride

Gene expression profiles of livers and liver tumors from mice fed high-fat diet and high fructose-glucose solution for 52 weeks

Project description:The lack of a preclinical model of nonalcoholic steatohepatitis (NASH) and hepatocellular cancer (HCC) that recapitulates human disease is a major barrier to therapeutic development. We report a high fat-high sugar diet-induced NASH and HCC in a stable isogenic 129S1/SvImJ crossed with C57Bl/6J mice. Following diet initiation, there was sequential development of steatosis (4-8 weeks), steatohepatitis with ballooning and Mallory-Denk bodies (12-16 weeks), progressive fibrosis (16 week onwards) and spontaneous HCC (32-52 weeks). The mice developed obesity, insulin resistance and dyslipidemia. There was concordance with the human NASH transcriptome (FDR 0.001) with activation of lipogenic, inflammatory and apoptotic pathways relevant in humans. The HCC gene signature resembled S1 and S2 human HCC subclass (FDR 0.01 for both). This simple model of NASH and HCC that resembles human disease in terms of its triggers, physiological and biochemical parameters, histology, transcriptomic profile, and outcomes can facilitate preclinical development for these conditions. 129S1/SvImJ;C57Bl/6J (129/B6) mice were fed with high-fat diet (Western Diet) and high fructose-glucose solution (Sugar Water) (WD SW) or chow diet (CD) for 52 weeks, and total RNA samples were isolated from liver and tumor tissues for genome-wide expression profiling.

2016-07-25 | E-GEOD-67679 | biostudies-arrayexpress

Gene expression profiles of livers from mice fed high-fat diet and high fructose-glucose solution for 8 weeks

Project description:The lack of a preclinical model of nonalcoholic steatohepatitis (NASH) and hepatocellular cancer (HCC) that recapitulates human disease is a major barrier to therapeutic development. We report a high fat-high sugar diet-induced NASH and HCC in a stable isogenic 129S1/SvImJ crossed with C57Bl/6J mice. Following diet initiation, there was sequential development of steatosis (4-8 weeks), steatohepatitis with ballooning and Mallory-Denk bodies (12-16 weeks), progressive fibrosis (16 week onwards) and spontaneous HCC (32-52 weeks). The mice developed obesity, insulin resistance and dyslipidemia. There was concordance with the human NASH transcriptome (FDR 0.001) with activation of lipogenic, inflammatory and apoptotic pathways relevant in humans. The HCC gene signature resembled S1 and S2 human HCC subclass (FDR 0.01 for both). This simple model of NASH and HCC that resembles human disease in terms of its triggers, physiological and biochemical parameters, histology, transcriptomic profile, and outcomes can facilitate preclinical development for these conditions. 129S1/SvImJ;C57Bl/6J (129/B6) mice were fed with high-fat diet (Western Diet) and high fructose-glucose solution (Sugar Water) (WD SW) or chow diet (CD) for 8 weeks, and total RNA samples were isolated from liver tissues for genome-wide expression profiling.

2016-07-25 | E-GEOD-67678 | biostudies-arrayexpress

Taste Receptor Type 1 Member 3 Mediates Cognitive Impairment in Diet-Induced Obese Mice

Project description:To investigate whether taste receptor type 1 member 3 (TAS1R3) might serve as a key modulator of cognitive impairment led by WD-induced obesity, male Tas1r3-wild type (WT) and knockout (KO) mice were randomized to receive either a normal diet (ND) or western diet (WD) for 18 weeks. We performed gene expression profiling analysis using data obtained from RNA-seq of hippocampus of two WT mice fed a WD (WT-WD) and two KO-WD mice.

2024-10-11 | GSE215332 | GEO

Transcriptome analysis of aortic valve tissues from hyperlipidemic and control mice with normal chow diet (chow) or western diet (WD)

Project description:We performed RNA sequencing of the aortic valves of C57BL/6J (the wild type with chow diet), Ldlr-/- (1. with chow diet, 2. with WD), and Apoe-/- mice (1. with chow diet, 2. with WD) to compare the overall transcriptomic characteristics within genetic differences (wild type, Ldlr-/-, Apoe-/-) or in dietary differences (chow diet versus WD).

2022-08-22 | GSE205587 | GEO

Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

Project description:Mice deficient in the LDL receptor (LDLR KO mice) fed with high fat diet (HFD) feeding have been widely used as a model to mimic human atherosclerosis. RNA-seq using aortic macrophages to investigate the effects of aortic macrophages on the plaque size progression. LDLR KO mice, 6-8 weeks old, were used, and fed with either an alternative HFD or a regular HFD. After aorta macrophages were isolated, RNeasy Mini Kit (Qiagen) was used to isolate mRNA. Single end (50bp), unstranded, SMART-Seq v4 plus nextera (SMART-Seq v4 Ultra Low Input RNA Kit (Takara) ). The RNA-seq libraries were prepared with SMART-Seq v4 Ultra Low Input RNA Kit (Takara).

2024-07-31 | E-MTAB-12759 | biostudies-arrayexpress

Changes in hepatic transcriptome profile in α4β7 mAb-treated Western diet-fed mice

Project description:Hepatic transcriptome of junctional adhesion molecule A knockout, F11r–/– mice fed a Western diet (WD) for eight weeks. A cohort of WD-fed mice were treated with IgG or α4β7 mAb for four weeks starting at week four following initiation of the WD.

2022-04-21 | GSE149208 | GEO

DNA microarrays of Wilson's disease patient-specific induced pluripotent stem cells

Project description:Wilson’s disease (WD) is a relevant human genetic disease caused by mutations in the ATP7B gene, whose product is a liver enzyme responsible for copper export into bile and blood. Interestingly, the spectrum of ATP7B mutations is vast and can influence clinical presentation (a variable spectrum of hepatic and neural manifestations), though the reason for this is not well understood. Here we describe the successful generation of iPSCs from a Chinese patient with Wilson’s disease that bears the R778L Chinese hotspot mutation in the ATP7B gene. Global gene expression profiling with DNA microarrays showed that WD iPSCs cluster together with human ESCs (H9) compared to donor fibroblasts. WD patient fibroblasts were isolated and expanded from a dermal biopsy of a middle age Chinese Han male, WD iPSCs were generated by overexpression of human Oct4/Sox2/Klf4/c-Myc in WD fibroblasts and expanded on Matrigel with mTESR1 culture medium. For DNA microarray analysis, WD fibroblasts (passage 5), 3 cell lines of WD iPSCs growing on Matrigel (passage 8) and human ES H9 growing on Matrigel (passage 40) were treated with Trizol, followed by RNA extraction and hybridization.

2010-12-01 | E-GEOD-24997 | biostudies-arrayexpress

Western diet triggers NLRP3-dependent persistent functional reprogramming of myeloid cells II [RNA-Seq]

Project description:Here we investigated whether sterile triggers of inflammation induce trained immunity and thereby influence innate immune responses. Western diet (WD) feeding of Ldlr-/- mice induced systemic inflammation, which was undectable in serum soon after mice were shifted back to chow diet (CD). In contrast, myeloid cell responses towards innate stimuli remained broadly augmented. WD induced transcriptomic and epigenomic reprogramming of myeloid progenitor cells, leading to increased proliferation as well as enhanced innate immune and interferon responses towards in vivo LPS challenge. QTL analysis in human monocytes trained with oxidized low-density lipoprotein (oxLDL) and stimulated with LPS suggested inflammasome-mediated trained immunity. Consistently, Nlrp3-/-/Ldlr-/--deficient mice lacked WD-induced systemic inflammation or myeloid progenitor proliferation and reprogramming. Hence, NLRP3 mediates trained immunity following WD and could thereby arbitrate the potentially deleterious effects of trained immunity in inflammatory diseases.

2018-01-17 | GSE106789 | GEO

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