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TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE130627 | GEO | 2019/12/21

REPOSITORIES: GEO

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Similar Datasets

TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [bulk RNA-seq]

Project description:TREM2 is a microglial-specific gene implicated in late-onset Alzheimer's Disease (AD). Recent studies have identified that Trem2-deficient mice exhibit transcriptional changes in microglial gene expression that minimize the upregulation of lipid metabolism and lysosomal genes in AD disease models. We find that chronic phagocytic challenge from demyelination generates similiarly attenuated expression of lysosomal and lipid metabolism genes in microglia isolated from Trem2 knockout mouse brain.

2019-12-21 | GSE124266 | GEO

TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [single-cell RNA-Seq]

2019-12-21 | GSE130626 | GEO

TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge

Project description:TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge

| PRJNA540829 | ENA

TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [bulk RNA-seq]

Project description:TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [bulk RNA-seq]

| PRJNA511441 | ENA

TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [single-cell RNA-Seq]

Project description:TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [single-cell RNA-Seq]

| PRJNA540830 | ENA

Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism.

Project description: Not available

| S-EPMC6554672 | biostudies-literature

Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism

Project description: Not available

| S-SCDT-EMM-2018-09711 | biostudies-other

TREM2 regulates microglial lipid metabolism during aging in mice [RNA-Seq]

Project description:TREM2 is a microglial-specific gene implicated in late-onset Alzheimer's Disease (AD). Recent studies have identified that Trem2-deficient mice exhibit transcriptional changes in microglial gene expression that minimize the upregulation of lipid metabolism and lysosomal genes in AD disease models. We detect similiarly attenuated expression of lipid metabolism genes in microglia isolated from brains of aged Trem2 knockout mice.

2019-12-21 | GSE134031 | GEO

TREM2 regulates microglial cell activation in response to demyelination in vivo.

Project description: Not available

| S-EPMC4667728 | biostudies-literature

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

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