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Age-associated modulation of TREM1/TREM2 expressing macrophages promotes melanoma progression and metastasis

ABSTRACT: Age-associated modulation of TREM1/TREM2 expressing macrophages promotes melanoma progression and metastasis

PROVIDER: PRJNA1179868 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31157033_1.fastq.gz	Fastqsanger.gz
	SRR31157033_2.fastq.gz	Fastqsanger.gz
	SRR31157034_1.fastq.gz	Fastqsanger.gz
	SRR31157034_2.fastq.gz	Fastqsanger.gz
	SRR31157035_1.fastq.gz	Fastqsanger.gz

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Age-associated modulation of TREM1/TREM2 expressing macrophages promotes melanoma progression and metastasis

Project description:Aging is a known risk factor for melanoma, yet the mechanisms underlying melanoma progression and metastasis in the older population remain largely unexplored. Among remaining gaps is the role of changes in melanoma microenvironment in key phenotypes exacerbated by age. Here we demonstrate that age enriches immunosuppressor tumor microenvironment which can be linked with melanoma metastasis phenotype. Age-associated macrophages with a tolerogenic phenotype and dysfunctional CD8 positive cells with an exhausted phenotype were identified in melanomas of aged mice and human. Macrophages of the older population were enriched of the immunosuppressor subcluster expressing Trem2 while the profibrotic subcluster expressing Trem1 was reduced. Notably, inhibition of TREM1 decreased melanoma growth in young but not old mice, whereas inhibition of TREM2 prevented lung metastasis in aged mice. These data identify novel targets in melanoma metastasis which may guide aged-dependent immunotherapies.

2025-02-27 | GSE280640 | GEO

TREM1 deficiency alters the tumor myeloid landscape

Project description:To comprehensively characterize the impact of TREM1 deficiency specifically within the tumor myeloid populations, we selectively enriched the CD45+CD11b+ tumor-infiltrating myeloid cells from tumor-bearing Trem1+/+ and Trem1-/- mice for scRNA-seq analysis.

2023-09-27 | E-MTAB-13246 | biostudies-arrayexpress

scRNA seq analysis of CD45+ tumor infiltrating cells (TICs) of B16F10 tumor-bearing Trem1+/+ and Trem1-/- mice.

Project description:To gain a global understanding of the impact of TREM1 silencing, we analyzed the CD45+ tumor infiltrating cells (TICs) of B16F10 tumor-bearing Trem1+/+ and Trem1-/- mice. Utilizing the 10x Genomics Chromium Platform, we analyzed approximately 5390 cells per sample with a coverage rate of 15493 genes per cell.

2023-09-27 | E-MTAB-13237 | biostudies-arrayexpress

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

Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages

Project description:Dipeptidyl peptidase 4 (Dpp4) plays a pivotal role in fibrotic and nonfunctional scar development following skin injury and is present in a subset of fibroblasts implicated in scar formation. Simultaneously, heterogeneous vascular endothelial cells (ECs) retain their capacity to drive tissue regeneration and repair within scarred areas. Effective strategies for inhibiting scar-associated fibroblasts and regulating EC subtypes in the scar microenvironment remain unclear. Here, we engineered CAR-Trem2-Ms capable of targeting DPP4+ fibroblasts and modulating EC phenotypes within the scar microenvironment to effectively prevent and treat scarring. Furthermore, compared to those in normal control samples, DPP4 expression levels were higher in both clinical scar databases and samples from scar patients. We transferred a CAR gene specifically targeting Dpp4+ fibroblasts into macrophages, which were then induced into CAR-Trem2-Ms with 1,25-dihydroxycholecalciferol (an active form of VD, VD3). Hydrogel micropore microneedles (mMNs) were employed to deliver CAR-Trem2-Ms to effectively alleviate scar formation. Single-cell transcriptome sequencing and analysis revealed that CAR-Trem2-Ms could modify EC phenotypes and regulate fibrosis by suppressing the profibrotic gene Lrg1. CAR-Trem2-Ms effectively inhibited fibrosis in fibroblasts induced by high EC LRG1 expression in vitro, further revealing the underlying mechanism by which CAR-Trem2-Ms exert their antifibrotic effects. Our findings offer a promising approach for treating post-traumatic scarring and provide novel insights into the pathological mechanisms underlying fibrosis.

2024-09-24 | GSE248759 | GEO

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

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

Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages

Project description:Scar management through modulation of the fibrotic microenvironment by CAR-Trem2-macrophages

| PRJNA1045715 | ENA

Pharmacological inhibition of TREM1 attenuates patient derived xenograft models

Project description:To characterize the transcriptional changes in PDX tumors during TREM1 inhibition by microarray

2023-09-27 | E-MTAB-13257 | biostudies-arrayexpress