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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (scRNA-Seq)

ABSTRACT: The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (scRNA-Seq)

PROVIDER: PRJNA977695 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24768000_1.fastq.gz	Fastqsanger.gz
	SRR24768000_2.fastq.gz	Fastqsanger.gz
	SRR24768001_1.fastq.gz	Fastqsanger.gz
	SRR24768001_2.fastq.gz	Fastqsanger.gz
	SRR24768002_1.fastq.gz	Fastqsanger.gz

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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury

Project description:The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury

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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury II

Project description:The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury II

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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (bulk RNA-Seq)

Project description:The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (bulk RNA-Seq)

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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury

Project description:We show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury.

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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury II

Project description:We show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury and ripasudil treatment.

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The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (scRNA-Seq)

Project description:We show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury.

2023-09-30 | GSE233749 | GEO

The GPR84 molecule is a mediator of a subpopulation of retinal microglia that promote TNF/IL-1α expression via the rho-ROCK pathway after optic nerve injury (bulk RNA-Seq)

Project description:We show that microglial gene expression patterns gradually change during RGC degeneration induced by optic nerve injury.

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The important role of GPR84 in MLL leukemogenesis

Project description:Beta-catenin signaling is required for establishment of leukemic stem cells (LSCs) in acute myeloid leukemia (AML), yet the upstream regulators that can augment this pathway are unknown. Through genome-wide gene expression analysis and functional studies, we identified an important role for GPR84 in MLL AML. Suppression of GPR84 significantly inhibited cell growth in pre-LSCs, reduced LSC frequency and impaired reconstitution of MLL AML. Furthermore, GPR84 conferred a growth advantage to Hoxa9/Meis1a transduced hematopoietic stem cells (HSCs). Our microarray analysis demonstrated that GPR84 overexpression significantly up-regulated a small set of MLL-fusion targets and beta-catenin co-effectors, and down-regulated a hematopoietic cell cycle inhibitor. These data thus reveal a previously unrecognized role of GPR84 in the maintenance of fully developed AML by sustaining aberrant beta-catenin signaling in LSCs. HSC-derived Hoxa9/Meis1a pre-LSCs were transduced with GPR84 cDNA or empty vector, and replated in methylcellulose supplemented with cytokines. Each group contains triplicate samples.

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Inhibition of Medium-Chain Fatty Acid Receptor GPR84 Enhances Metabolism, Cytotoxicity and Anti-Tumor Function of CD8 T cells

Project description:GPR84 is a medium-chain free fatty acid receptor predominately expressed on myeloid cells. Previous studies identified GPR84 as an enhancer of pro-inflammatory myeloid cell response and a regulator of metabolic homeostasis. However, the role of GPR84 on T cell function and metabolism remains wholly unexplored. This study tested the effect of GPR84 modulation on CD8+ T cell function and metabolism in vitro, and examined its effect on anti-tumor function in adoptive cellular therapy models. Inhibition of GPR84 with the antagonist GLPG1205 promoted CD8+ T cell differentiation, proliferation, cytokine production, and cytotoxicity. This effect was confirmed using CRISPR-Cas9 GPR84 deleted CD8+ T cells. In contrast, treatment with the GPR84 agonist DL175 inhibited proliferation, cytokine production and cytotoxicity. These functional changes were paralleled by changes in metabolic activity. GPR84 antagonist GLPG1205 increased glucose uptake, glycolysis, oxidative phosphorylation (OXPHOS) and ATP production, which enhanced the energetic fitness of CD8+ T cells. Furthermore, stimulation of antigen-specific CD8+ T cells with GPR84 antagonist in vitro, or deletion of GPR84 in antigen specific T cells before adoptive cellular therapy resulted in a significantly enhanced anti-tumor effect in vivo. This study is the first demonstration that GPR84 modulation in T cells can enable more effectively killing of tumor cells and reduce tumor growth, and opens a novel approach to significantly enhance the efficacy of adoptive cellular therapies including CAR-T, TIL or CAR-NK cells.

2025-12-26 | GSE241488 | GEO

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Project description:Ethnopharmacological relevance The traditional Chinese medicine Psoralea corylifolia L. (PCL) has been clinically used to treat diarrhea and gastrointestinal inflammatory disorders. G protein-coupled receptor 84 (GPR84) is emerging as a potential target for inflammatory bowel disease (IBD). Pharmacological investigations confirm the efficacy of PCL against IBD, but its active components targeting GPR84 and their mechanisms remain unclear. Aim of the study We aimed to identify active components from PCL against GPR84, evaluate their therapeutic effects and elucidate their mechanisms of action in IBD treatment.

2025-09-28 | GSE305628 | GEO

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