Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1082619 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Exposure to PFOA during gestation altered the expression of genes related to fatty acid catabolism in both the fetal liver and lung. In the fetal liver, the effects of PFOA were robust and also included genes associated with lipid transport, ketogenesis, glucose metabolism, lipoprotein metabolism, cholesterol biosynthesis, steroid metabolism, bile acid biosynthesis, phospholipid metabolism, retinol metabolism, proteosome activation, and inflammation. These changes are consistent with activation of PPAR alpha. Non-PPAR alpha related changes were suggested as well. Keywords: gene expression, microarray,PFOA, mouse, fetus, liver
2008-10-07 | GSE13044 | GEO
Project description:"Liver represents one of the most important organs involved in the elimination of xenobiotic and potentially toxic substances. Cigarette smoke (CS) contains more than 7000 chemicals, among which compounds that exert biological effects and cause smoking-related diseases. Although CS is not directly hepatotoxic, a growing body of evidence suggests that it may exacerbate (pre-existing) chronic liver diseases. Here we integrated toxicological endpoints with molecular measurements and computational analysis approaches to investigate exposure effects on liver in an Apoe-/- mouse study. The mice were exposed to high concentrations of 3R4F reference CS (600 mg/m3 TPM, 29.9 mg/m3 nicotine), an aerosol from a candidate reduced risk product (RRP) the Tobacco Heating System (THS) 2.2 at matching nicotine concentration, or filtered air (Sham) for up to 8 months. THS2.2 was conceived using the heat-not-burn technology that heats tobacco avoiding pyrogenesis and pyrosynthesis. After 2 months of CS exposure, some groups were either switched to the RRP or underwent exposure cessation. While clear signs of hepatotoxic effects were absent for any exposure group, the integrative analysis of proteomics and transcriptomics data showed a CS-dependent impairment of specific biological networks, including lipid and xenobiotic metabolism, and iron homeostasis, which likely in turn mutually contribute to worsening of the oxidative stress. In contrast, most of these changes were absent in mice exposed to THS2.2, and in the cessation and switching groups. Our findings shed light on the complex biological response of the liver to CS exposure and support the benefits of switching to the tested heat-not-burn product, THS2.2."
2016-12-22 | PXD002925 | Pride
Project description:Microplastics (MPs) have become a serious global environmental threat that causes damage to mammalian organs. In this work, we investigated the potential molecular mechanism underlying the development of liver fibrosis induced by long-term exposure to three different sized PS-MPs (80 nm, 0.5 µm and 5 µm) in mice. Liver fibrosis levels were evaluated in mice after chronic exposure to PS-MPs. Liver inflammation was mainly increased in chronic exposure to 80 nm and 0.5 µm PS-MPs. Liver lipid deposition was significantly enhanced after PS-MP exposure. However, oxidative stress was not changed under PS-MP exposure. GO enrichment and KEGG pathway analyses revealed that the DEGs and shared DEGs were mainly enriched in the metabolism of lipids. The mRNA expression levels of genes related to fatty acid oxidation, synthesis and transport were dramatically induced by PS-MP exposure. Four hub genes, Acot3, Abcc3, Nr1i3 and Fmo2, were identified by CytoHubba analysis of shared DEGs. The mRNA expression levels of three hub genes, Acot3, Abcc3 and Nr1i3, were significantly augmented under chronic PS-MP exposure. Our results suggest that Acot3, Abcc3 and Nr1i3 are potential molecules involved in the development of liver fibrosis under chronic exposure to PS-MPs.
2025-01-23 | GSE245069 | GEO
Project description:The contamination of marine ecosystems with microplastics, such as the polymer polyethylene, a commonly used component of single-use packaging, is of global concern. Although it has been suggested that biodegradable polymers, such as polylactic acid, may be used to replace some polyethylene packaging, little is known about their effects on marine organisms. Blue mussels, Mytilus edulis, have become a “model organism” for investigating the effects of microplastics in marine ecosystems. We show here that repeated exposure, over a period of 52 days in an outdoor mesocosm setting, of M. edulis to polyethylene microplastics reduced the number of byssal threads produced and the attachment strength (tenacity) by ~50%. Exposure to either type of microplastic altered the haemolymph proteome and, although a conserved response to microplastic exposure was observed, overall polyethylene resulted in more changes to protein abundances than polylactic acid. Many of the proteins affected are involved in vital biological processes, such as immune- and stress- regulation, metabolism and cellular and structural development. Our study highlights the utility of mass spectrometry-based proteomics to assess the health of key marine organisms and identifies the potential mechanisms by which microplastics, both conventional and biodegradable, could affect their ability to form and maintain reefs.
2019-01-02 | PXD011567 | Pride
Project description:Genome wide association studies of plasma lipid traits suggest a potential link between ILRUN and plasma cholesterol homeostasis. In this study, we sought to study the in vivo role of ILRUN in lipid metabolism. The transcriptional effects of Ilrun deficiency on mouse liver was unknown. We isolated livers from control and global IlrunKO mice for transcriptomic profiling.
2020-09-11 | GSE156151 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the effects of liver-specific E4BP4 overexpression under mouse albumin promoter on the liver glucose and lipid metabolism.
2024-03-31 | GSE183079 | GEO
Project description:Polybrominated diphenyl ethers (PBDEs) were used as flame-retardant additives starting 1965 and were recently withdrawn from commerce in North America and Europe. Approximately 1/5 of the total U.S. population were born when environmental concentrations of PBDE plateaued at their maximum. Accumulating evidence suggests that developmental exposures to PBDE may result in long-lasting programming of liver metabolism. In this study, CD-1 mice were exposed prenatally or neonatally to 1 mg/kg body weight of 2,2’,4,4’-tetrabromodiphenyl ether (BDE-47), and changes in liver gene histology, transcriptome, and liver-blood balance of triglycerides were analyzed in 10 month old male offspring. In both exposure groups, long-term reprogramming of lipid metabolism was observed, including increased liver triglycerides and decreased blood triglycerides, and altered expression of metabolic genes in the liver. Significant upregulation of lipid influx transporter Cd36 2.3- and 5.7-fold in pre- and neonatal exposure groups respectively was identified as a potential mechanism of blood/liver imbalance of triglycerides. Analysis of our and previously published all-genome gene expression data identified changes in expression of ribosomal protein genes as a transcriptomic signature of PBDE exposure. Further comparison of our new data and published data demonstrate that low doses (0.2 mg/kg body weight) of PBDE induce long-lasting up-regulation of ribosomal genes, suppression of Cd36 in liver and increase circulating triglycerides in blood, while moderated doses (≥ 1 mg/kg body weight) produce opposite long-lasting effects. To conclude, this study shows that an environmentally relevant developmental exposures to BDE-47 permanently alter lipid uptake and accumulation in the liver, with low and moderate doses having opposite effect on liver transcriptomics and triglyceride balance. Similar effects of pre- and neonatal exposures point at hepatocyte maturation as a sensitive window of the liver metabolism programming. These results suggest that PBDE exposure may be an important factor increasing risks of cardio-vascular disease and non-alcoholic fatty liver disease. The translational relevance of these findings for human remain to be studied.
2019-07-19 | GSE115143 | GEO
Project description:Microplastics (MPs) are considered as one of the main reasons for male and female infertility. However, the reproductive toxicity and its related mechanisms are understood by animal models with acute exposure to MPs at present. In the study, we show the low-dose polystyrene microplastics (PSMPs) exposure results in severely abnormal reproduction in female, but not male in mouse model, exhibiting failed oocyte meiotic maturation. Mechanistically, the PSMPs exposure induces the over-activation of cell metabolism pathways, insufficient HDACs and H4K16 hyperacetylation in oocytes in vivo and in vitro. By addition of HDAC3 inhibitor, the failed oocyte maturation, over-activation of cell metabolism pathways and H4K16 hyperacetylation are recapitulated, and the overexpression of HDAC3 can rescue the defects of meiotic maturation induced by PSMPs. Our observations suggest a direct link of the maturation defects induced by PSMPs to HDAC3 insufficiency. Thus, we propose the potential treatments for therapy of the failed meiotic maturation of oocyte from women highly exposed to MPs by activating or supplying HDAC3.
2024-03-06 | GSE259264 | GEO
Project description:Dietary fiber such as inulin have been reported to promote cardiovascular and metabolic health. However, the mechanisms involved are not well understood. We studied effects of inulin on lipid metabolism in Ldlr deficient atherosclerosis mouse model using lipidomics and transcriptomics. Plasma and tissues were collected at 10 days and/or 12 weeks after feeding an atherogenic diet supplemented with inulin or cellulose (control).
2020-01-02 | E-MTAB-8259 | biostudies-arrayexpress