RNA sequencing data of liver macrophages from ND/WD mice
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ABSTRACT:
PROVIDER: PRJNA816087 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:RNA seq from the liver, ileum, muscle, fat of SPF or GF mice on ND, WD. "Microbiota and adipocyte mitochondrial damage in type 2 diabetes are linked by Mmp12+ macrophages"
2022-05-13 | GSE145052 | GEO
Project description:Genes expression profile in liver macrophages isolated from wild type C57BL/6J mice fed either a western diet or normal diet
2022-12-06 | GSE198595 | GEO
Project description:Purpose: Excessive intake of a western diet (WD), characterized by high fat and sugary drinks, is hypothesized to contribute to the development of inflammatory bowel disease (IBD). Despite the identified clinical association, the molecular mechanisms through which dietary changes lead to IBD development remain unknown. Here, we generated a murine model of severe intestinal inflammation triggered by long-term WD consumption, which exhibited markedly elevated taste receptor TAS1R3 expression in inflamed bowel tissues. Thus, we hypothesized that nutrient-induced TAS1R3 modulation is central to regulating intestinal inflammation. We tested our hypothesis by analyzing changes in gene expression profiles and inflammatory cell infiltration in the inflamed bowel tissues of WD-fed Tas1r3-deficient mice. Methods: We carried out RNA-Seq of ileum tissue of wild-type (WT) and taste receptor Tas1r3 knockout (Tas1r3−/−) mice fed a normal diet (ND) or western diet (WD) for 10 weeks using Ion Proton System. Raw RNA-seq reads were split into individual samples based on barcodes and quality controlled using the FASTQC tool. The reads were analyzed with Partek Flow software (Partek, St. Louis, MI, USA) (http://www.partek.com/partekgs). The sequence reads that passed quality filters were analyzed at the transcript isoform level. Results: We confirmed that Tas1r3-deficient mice are protected from WD-induced intestinal inflammation. Consistent with little or no phenotypic change in the ND group, the gene expression profiles from the ND-fed Tas1r3−/− and WT mice were similar, whereas the ileal transcriptome profiles from the WD-fed Tas1r3−/− mice were readily distinguishable from those of WD-fed WT mice. Inflammatory cytokines such as Tnfα and Il1b were highly expressed in WD-fed WT mice, whereas Pparg, Tjp3, and Defa27 were highly expressed in WD-fed Tas1r3−/− mice. Importantly, we confirmed that the absence of TAS1R3 caused a significant reduction in the inflammatory response-related signaling pathway; GSEA plots also revealed that the mTOR signaling pathway was greatly suppressed. Most notably, the PPAR signaling pathway was significantly affected by TAS1R3 absence. GSEA confirmed that genes associated with the PPAR signaling pathway were significantly enriched in the set of DEGs between Tas1r3−/− and WT mice in the WD groups. Conclusion: Our data suggest that, due to its suppressive action on mTOR, TAS1R3 might function as an important regulator of the PPAR-γ signaling pathway in the intestinal tract.
2023-04-19 | GSE190059 | GEO
Project description:RNA-seq from the liver and ileum of mice on ND, WD, and WD with either Lactobacillus gasseri or Lactobacillus johnsonii
| PRJNA560977 | ENA
Project description:RNA-seq from the liver, ileum, muscle, fat of SPF or GF mice on ND, WD
| PRJNA605809 | ENA
Project description:Transcriptional profiling for screening olfactory receptor expressions in C57BL/6J mouse liver and adipose tissue under either ND and HFD
2017-08-24 | GSE102977 | GEO
Project description:Wildtype (WT) and albumin-knockout (AKO) were fed with normal diet. We harvested the liver tissues from WT and AKO mice at 3-week, 8-week, and 10-month of age. We then performed gene expression profiling analysis using data obtained from RNA-seq of the six different liver tissues. Wildtype (WT) and albumin-knockout (AKO) mice were fed with Normal diet (ND) or Western diet (WD) for 8 weeks from the age of 8 weeks. We harvested the liver tissues from WT-ND, WT-WD, AKO-ND, AKO-WD mice . We then performed gene expression profiling analysis using data obtained from RNA-seq of the four different liver tissues. Wildtype (WT) mice fed with HFD from the age of 8 weeks were injected by 17-AAG at the 3rd, 4th, 5th, 6.5th, and 8th weeks of the HFD feeding process. The control group was injected by the solvent. Another group of mice at the same age was fed with normal diet (ND). We harvested the liver tissues ND, Ctrl, and 17-AAG mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of the three different liver tissues.
2023-01-20 | GSE222922 | GEO
Project description:Intestinal transcriptome profiles of ND and WD-fed Tas1r3−/− and Wild Type mice using RNA-seq analysis
| PRJNA785649 | ENA
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
Project description:RNA sequencing data of liver macrophages
| PRJNA811586 | ENA