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Transcriptomic profiling of isolated hepatic macrophage subsets (Kupffer cells, Monocyte-derived Macrophages and Monocytes) in common bile duct ligated (CBDL)-mice, mice with acute colitis (DSS), and combinations (CBDL+DSS)

ABSTRACT: Transcriptomic profiling of isolated hepatic macrophage subsets (Kupffer cells, Monocyte-derived Macrophages and Monocytes) in common bile duct ligated (CBDL)-mice, mice with acute colitis (DSS), and combinations (CBDL+DSS)

PROVIDER: PRJNA761692 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15812113.fastq.gz	Fastqsanger.gz
	SRR15812114.fastq.gz	Fastqsanger.gz
	SRR15812115.fastq.gz	Fastqsanger.gz
	SRR15812116.fastq.gz	Fastqsanger.gz
	SRR15812117.fastq.gz	Fastqsanger.gz

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Transcriptomic profiling of isolated hepatic macrophage subsets (Kupffer cells, Monocyte-derived Macrophages and Monocytes) in common bile duct ligated (CBDL)-mice, mice with acute colitis (DSS), and combinations (CBDL+DSS)

Project description:In this study, we aimed to unravel the transcriptional profiles of specific hepatic macrophage subsets during cholestatic liver injury, acute colitis and when colitis is induced as a second hit on advanced cholestatic liver injury. Differentially expressed genes (DEGs) and corresponding pathways were determined via DESeq2 in R and STRING-App comparing groups or cell types as outlined in the 'overall design' section below. Our results highlight the heterogeneity of the liver macrophage (MF) pool and describe functional differences between MF subsets. Longitudinally, the CBDL-associated expression profiles of each macrophage subset remained mostly stable. CBDL-induced cholestatic liver injury was characterized by the emergence of Trem2/Spp1 expressing monocyte-derived macrophages (MoMFs). DSS-colitis as a second hit on cholestatic liver injury enhanced this phenotype of MoMFs.

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NorUrsodeoxycholic Acid Ameliorates Cholemic Nephropathy in Common Bile Duct Ligated Mice

Project description:Cholestasis may cause cholemic nephropathy that can be modelled in common bile duct ligated (CBDL) mice. We aimed to explore the therapeutic efficacy and mechanisms of norursodeoxycholic acid (norUDCA) in cholemic nephropathy. To determine whether norUrsodeoxycholic acid (norUDCA) prevents cholemic nephropathy in long-term CBDL mice, a norUDCA-enriched diet (0.125% w/v, corresponding to 200 mg/kg/day for a mouse of 25 g body weight eating about 4g daily) or a standard mouse diet (Sniff, Soest, Germany) were started 5 days prior to CBDL and were continued until harvesting 3 weeks thereafter. For transcriptional profiling using microarray technology, we compared sham-operated (SOP) mice and 3-week CBDL mice that were either fed 0.125% norUDCA-enriched or standard mouse diets.

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DSS induced colitis mice Astral-DIA

Project description:This study aims to investigate the protein expression profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis using advanced Astral-DIA quantitative proteomics technology. A total of 12 colon tissue samples were analyzed, including 6 from healthy control mice and 6 from DSS-treated mice with induced colitis. Experimental Design Species: Mus musculus (C57BL/6 strain). Tissue Source: Colon tissues were dissected, snap-frozen in liquid nitrogen, and homogenized to extract proteins. Groups: Control Group: Healthy mice without intervention. DSS Group: Mice subjected to 2.5% DSS administration for 7 days to induce colitis, validated by histopathological assessment.

2025-09-18 | PXD063633 | Pride

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- miRNA microarray

Project description:To find out which miRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed miRNA microarray as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The miRNA microarray experiments were performed together.

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Project description:To find out which mRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The whole genome microarray expression profiling experiments were performed together.

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Project description:Adamts12-deficient mice undergo more severe colitis than WT mice after induction with DSS. We used microarrays to determine the gene expression differences between Adamts12-deficient and WT mice during ulcerative colitis induced with DSS (dextran sodium sulfate) Fragments of distal colon from DSS-treated (2% DSS during 7 days and 1 day of recovery) and untreated Adamts12-deficient and WT mice were obtained for RNA extraction and hybridiztion with Affymetrix microarrays

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Mandibular and Femur-Derived Ligated preosteoclasts from LSD1WT and cKO mice

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The ligation between ERMAP, galectin-9 and dectin-2 promotes Kupffer cell phagocytosis and antitumor immunity

Project description:The innate immune system functions as the first line of defense against cancer cells, particularly the detection and clearance of cancer cells by phagocytosis. The liver resident macrophages, known as Kupffer cells, have the largest population of body’s tissue resident macrophages and constitute the first line of defense against cancer cells invading the liver. However, the molecule mechanisms underlying the detection and phagocytosis of cancer cells by Kupffer cells are still unclear. Here, using in vivo genome-wide CRISPR-Cas9 knockout screening, we found that Ermap expressed on cancer cells delivered the pro-phagocytosis ‘eat me’ signal to promote Kupffer cells phagocytosis and control over liver metastasis of various cancer cells. Ermap ligated Galectin-9 expressed on Kupffer cells surface in a glycosylation dependent manner. Galectin-9 further formed a bridging complex with Ermap and transmembrane receptor Dectin-2 expressed on Kupffer cells to promote the detection and phagocytosis of cancer cells by Kupffer cells. Patients with tumors expressing low ERMAP had more liver metastases. Thus, our study identifies the Ermap–Galectin-9–Dectin-2 axis as an ‘eat me’ signal for Kupffer cells to engulf cancer cells and control liver metastasis.

2023-08-03 | GSE232126 | GEO

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- miRNA microarray

2013-05-10 | GSE44983 | GEO

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Project description:Abstract. Ulcerative colitis (UC) is an intestinal disease characterized by chronic recurrent inflammation, but the underlying mechanism remains undefined and requires in-depth exploration. The aim of the present study was to investigate the biological effects of a small molecular compound M1002 of oxygen-sensing signaling pathway on dextran sulfate sodium (DSS)-induced intestinal inflammation colitis mouse models. It was found that the protective effects of M1002 on DSS-induced colitis. To determine how M1002 exerted its protective effect in DSS-induced colitis, we compared the global gene expression profiles in the gut between DSS control and M1002 treatment colitis mouse groups by RNA-Seq. The results demonstrated that HIF-1 signaling pathway-related genes were significantly upregulated in the gut of M1002 treatment colitis mice, whereas the Inflammatory bowel disease signaling pathway, the TNF signaling pathway, and Cytokines and inflammatory response signaling pathway related genes were significantly downregulated in the M1002 treatment group. 16S rRNA gene sequencing demonstrated remarkable variations in the composition of gut microbiota between DSS control and M1002 treatment colitis mice. Compared with DSS control colitis mice, the relative abundance of Eubacterium_nodatum and Halomonas in the gut microbiota was significantly increased at genus level in the gut of M1002 treatment colitis mice. Based on these findings, we tend to conclude that M1002 might alleviate DSS-induced gut injury in mice by regulation of HIF-1 signaling and up-regulating Eubacterium_nodatum and Halomonas.

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