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Single cell sequencing of murine hepatic CD45+ cells from mice transplanted with Trem2-deficient or wild-type bone marrow with NASH

ABSTRACT: We report the single cell transcriptome of CD45+ cells from the livers of bone marrow chimeric wildtype mice with NASH that had previously been transplanted with bone marrow from TREM2-deficient or wildtype littermate mice. We show that hematopoietic TREM2 deficiency is associated with alterations in the hepatic immune cell composition in the context of NASH.

ORGANISM(S): Mus musculus

PROVIDER: GSE207138 | GEO | 2022/07/01

REPOSITORIES: GEO

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Single cell sequencing of murine hepatic CD45+ cells from mice transplanted with Trem2-deficient or wild-type bone marrow with NASH

Project description:Single cell sequencing of murine hepatic CD45+ cells from mice transplanted with Trem2-deficient or wild-type bone marrow with NASH

| PRJNA853789 | ENA

scRNAseq profiling of lung myeloid cells in Trem2+/+ : Trem2-/- mixed bone marrow chimeric mice

Project description:scRNAseq profiling of FACS-sorted Trem2 +/+ (CD45.2+) and Trem2 -/- (CD45.1+) myeloid enriched (DAPI-CD45+Ly6G- CD3e-CD11b+ and/or CD11c+) fractions purified from KP-GFP bearing lungs (21 days after tumor delivery intravenously) isolated from mixed bone marrow chimeric mice.

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Lipid droplet-mediated danger signaling balances Trem2+ macrophage induction and NLRP3 inflammasome activation in NASH

Project description:Macrophages are exquisitely capable of sensing danger-associated molecular patterns (DAMPs) and orchestrating inflammatory response during tissue injury. Nonalcoholic steatohepatitis (NASH) represents an advanced stage of metabolic fatty liver disease that increases the risk for cirrhosis and liver cancer. Pathogenic mechanisms of NASH center on hepatocyte injury and the ensuing immune response within the liver microenvironment. However, the nature of DAMPs released by injured hepatocytes and how they shape the liver immune milieu remain largely unknown. Here we show that lipid droplets (LDs) released by injured fatty hepatocytes provide a potent signal that triggers monocyte infiltration and maturation into Trem2+ macrophages, recently described as NASH-associated macrophages (NAMs) or lipid- associated macrophages. LD treatment exacerbated liver injury in mice with diet-induced NASH. We identified Membrane spanning 4-domains a7 (Ms4a7) as a NAM-specific pathogenic factor that was strongly induced in mouse and human NASH. Ms4a7 inactivation ameliorated key aspects of diet-induced NASH pathologies in mice. At the mechanistic level, Ms4a7 physically interacts with NLR family pyrin domain containing 3 (NLRP3) and is required for endosomal NLRP3 inflammasome activation. These findings illustrate a crucial role of Ms4a7 in driving pro-inflammatory signaling in NASH liver. Surprisingly, LD treatments attenuated Ms4a7 expression and NLRP3 inflammasome activation in cultured macrophages. As such, LDs serve as a DAMP signal that balances the induction of Trem2+ macrophages and NLRP3 inflammasome activation in NASH liver

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Post-transplant (non-alcoholic steatohepatitis) NASH compared with transplanted normal controls

Project description:Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of disease that ranges from simple steatosis, to inflammatory form non-alcoholic steatohepatitis (NASH), cirrhosis, and up to hepatocellular carcinoma. While NASH usually takes decades to develop at a rate of one stage per seven years, in the case of post-trasplant NASH (pt-NASH) develops fibrosis much more rapidly, with almost 50% of liver transplant recipients presenting stage 3 fibrosis by 5 years post-transplant. Archived fresh-frozen transplanted liver biopsy samples from four liver biopsy samples with evidence of NASH (2 recurrent and 2 de novo), two with simple steatosis (both de novo), and five with normal histology as controls had their transcriptome sequenced in two batches for deeper coverage.

2022-05-09 | E-MTAB-11688 | biostudies-arrayexpress

NASH

Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays

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Gene expression profile of bone marrow derived M-CSF-dependent macrophage from Ogfrl1 KO mouse

Project description:To investigate the role of Ogfrl1 in macrophages, we isolated bone marrow derived M-CSF-dependent macrophages (BMMs) from femur and tibia of Ogfrl1 deficient mouse and wildtype littermate mouse.

2023-12-01 | GSE247888 | GEO

TREM2 regulates microglial cell activation in response to demyelination in vivo

Project description:Microglia are phagocytic cells that survey the brain and perform neuroprotective functions in response to tissue damage, but their activating receptors are largely unknown. Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial immunoreceptor whose loss-of-function mutations in humans cause presenile dementia, while genetic variants are associated with increased risk of neurodegenerative diseases. In myeloid cells, TREM2 has been involved in the regulation of phagocytosis, cell proliferation and inflammatory responses in vitro. However, it is unknown how TREM2 contributes to microglia function in vivo. Here, we identify a critical role for TREM2 in the activation and function of microglia during cuprizone (CPZ)-induced demyelination. TREM2-deficient (TREM2(-/-)) mice had defective clearance of myelin debris and more axonal pathology, resulting in impaired clinical performances compared to wild-type (WT) mice. TREM2(-/-) microglia proliferated less in areas of demyelination and were less activated, displaying a more resting morphology and decreased expression of the activation markers MHC II and inducible nitric oxide synthase as compared to WT. Mechanistically, gene expression and ultrastructural analysis of microglia suggested a defect in myelin degradation and phagosome processing during CPZ intoxication in TREM2(-/-) microglia. These findings place TREM2 as a key regulator of microglia activation in vivo in response to tissue damage. Two STAGE (6weeks 12 weeks),

2015-07-06 | E-GEOD-70475 | biostudies-arrayexpress

Transcriptomic analysis of injured and uninjured knee joints from Trem2 KO mice [bulk RNA-seq]

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2022-07-18 | GSE200842 | GEO

TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration

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2022-08-12 | PXD029429 | Pride

Expression data from WT and TREM2 deficient microglia in a mouse model of Alzheimer's disease

Project description:We examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease Microglia were FACS-purified from 8.5 month old WT, Trem2-/-, 5XFAD, and Trem2-/- 5XFAD mice

2015-03-13 | E-GEOD-65067 | biostudies-arrayexpress

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