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TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [scRNA-Seq]

ABSTRACT: TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [scRNA-Seq]

PROVIDER: PRJNA1179888 | ENA |

REPOSITORIES: ENA

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TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [bulkRNA-seq]

Project description:TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [bulkRNA-seq]

| PRJNA1179315 | ENA

TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [10 Visium Spatial Seq]

Project description:TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [10 Visium Spatial Seq]

| PRJNA1179316 | ENA

TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [bulkRNA-seq]

Project description:Analysis of single cell RNA-seq, CITE-seq data and bulk RNA-seq data on cells isolated from the livers of mice following PBS and APAP (paracetamol/acetaminophen) administration. Spatial Transcriptomics analysis was performed using 10x Visium platform on mouse livers 48hrs post PBS or APAP administration. We also analysed single cell RNA-seq data on CD64+F4/80+ macrophages isolated from the livers of Trem2 fl/fl mice and CD64CRE Trem2 fl/fl mice.

2024-10-30 | GSE280514 | GEO

TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [scRNA-Seq]

2024-10-30 | GSE280652 | GEO

TREM2 expression delineates spatially restricted and ontogenically distinct hepatic macrophages populations required for tissue repair. [10 Visium Spatial Seq]

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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

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

Project description:Triggering receptor expressed on myeloid cell 2 (TREM2) is linked to neurodegenerative disease risk. However, the function of TREM in neurodegeneration is still unclear. Here we investigated the role of microglial TREM2 in TAR-DNA binding protein 43 kDa (TDP-43)-related neurodegeneration using viral-mediated and transgenic mouse models. We found that TREM2 deficiency impaired phagocytic clearance of pathological TDP-43 by microglia, and enhanced neuronal damage and motor impairments. Mass cytometry analysis revealed that hTDP-43 induced a TREM2-dependent subpopulation of microglia with high CD11c expression and phagocytic ability. Using mass spectrometry and surface plasmon resonance analysis, we further demonstrated an interaction between TDP-43 and TREM2 in vitro and in vivo as well as in ALS patient tissues. We computationally identified the region within hTDP-43 that interacts with TREM2. Our data highlights that TDP-43 is a possible ligand for microglial TREM2 and that this interaction mediates neuroprotection effects of microglia in TDP-43-related neurodegeneration.

2022-08-12 | PXD029429 | Pride

Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (expression)

Project description:Interactions between the nuclear lamina (NL) and chromatin are thought to occur through large lamin association domains (LADs) and correlate with gene repression in these domains. We show that binding of lamin A/C (LMNA) to promoters occurs on discrete domains that are associated with distinct transcriptional outputs. Chromatin immunoprecipitation identifies thousands of LMNA-bound promoters, primarily linked to signaling functions. LMNA often occupies narrow domains on promoters, yet LMNA-bound promoters are often contiguous. LMNA-bound genes are overall repressed, but repression correlates with co-enrichment in repressive histone marks rather than LMNA occupancy per se. Genes marked by LMNA and H3K4me3 escape LMNA-associated repression in the absence of repressive histone marks. Positioning of LMNA on promoters relative to the TSS correlates with distinct transcriptional outputs: whereas upstream-distal binding can be transcriptionally permissive, TSS occupancy is associated with promoter inactivity. Perturbation in NL organization causes reorganization of lamin promoter occupancy and uncouples LMNA binding from promoter inactivity. Our results show the existence of many spatially restricted LMNA binding events on promoter regions, with distinct position-dependent transcriptional outputs. Total RNA obtained from ASCs and ASCs depleted of LMNA (LMNA-KD) and processed for microarray hybridization.

2013-07-14 | E-GEOD-42523 | biostudies-arrayexpress

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

Expression data from wild type (WT) and TREM2 null alveolar macrophages (AM)

Project description:TREM-2 has been described to be a phagocytic receptor. We assessed the influence of TREM-2 on gene expression in alveolar macrophages (AM) In this data-set we characterised the differences in basal gene expression using affymetrix mouse 1.0 ST arrays between WT and TREM2-/- AM and observed TREM2 -/- AM to exhibt higher expression of opsonins 4 samples were analysed in biological duplicate (2 x WT and 2 x TREM2-/-)

2015-01-01 | E-GEOD-51378 | biostudies-arrayexpress

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