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Cannabinoid receptor 2 is necessary to induce toll-like receptor-mediated microglial activation.

ABSTRACT: Cannabinoid receptor 2 is necessary to induce toll-like receptor-mediated microglial activation.

PROVIDER: PRJNA725205 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14325859.fastq.gz	Fastqsanger.gz
	SRR14325860.fastq.gz	Fastqsanger.gz
	SRR14325861.fastq.gz	Fastqsanger.gz
	SRR14325862.fastq.gz	Fastqsanger.gz
	SRR14325863.fastq.gz	Fastqsanger.gz

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Cannabinoid receptor 2 is necessary to induce toll-like receptor-mediated microglial activation.

Project description:The tight regulation of microglia activity is key for precise responses to potential threats, while uncontrolled and exacerbated microglial activity is neurotoxic. Microglial toll-like receptors (TLRs) are indispensable for sensing different types of assaults and triggering an innate immune response. Cannabinoid receptor 2 (CB2) signaling is a key pathway to control microglial homeostasis and activation, and its activation is connected to changes in microglial activity. We aimed to investigate how CB2 signaling impacts TLR-mediated microglial activation. Here, we demonstrate that deletion of CB2 causes a dampened transcriptional response to prototypic TLR ligands in microglia. Loss of CB2 results in distinct microglial gene expression profiles, morphology, and activation. We show that the CB2-mediated attenuation of TLR-induced microglial activation is p38 MAPK-dependent. Taken together, we demonstrate that CB2 expression and signaling are necessary to fine-tune TLR-induced activation programs in microglia.

2021-08-23 | GSE173337 | GEO

Microglial cannabinoid receptor type 1 mediates social memory deficits produced by adolescent THC exposure and 16p11.2 duplication

Project description:Adolescent cannabis use increases the risk for cognitive impairments and psychiatric disorders. Cannabinoid receptor type 1 (Cnr1) is expressed not only in neurons and astrocytes, but also in microglia, which shape synaptic connections during adolescence. Nonetheless, until now, the role of microglia in mediating the adverse cognitive effects of delta-9-tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis, has been unexplored. Here, we report that adolescent THC exposure produces microglial apoptosis in the medial prefrontal cortex (mPFC), which was exacerbated in the mouse model of 16p11.2 duplication, a representative copy number variation (CNV) risk factor for psychiatric disorders. These effects are mediated by microglial Cnr1, leading to reduction in the excitability of mPFC pyramidal-tract neurons and deficits in social memory in adulthood. Our findings highlight the importance of microglial Cnr1 to produce the adverse effect of cannabis exposure in genetically vulnerable individuals.

2023-10-03 | GSE242892 | GEO

MICROGLIAL CELL EXPRESSION OF THE TYPE 2 CANNABINOID RECEPTOR REGULATES IMMUNE-MEDIATED NEUROINFLAMMATION

Project description:MICROGLIAL CELL EXPRESSION OF THE TYPE 2 CANNABINOID RECEPTOR REGULATES IMMUNE-MEDIATED NEUROINFLAMMATION

| PRJNA1063329 | ENA

MICROGLIAL CELL EXPRESSION OF THE TYPE 2 CANNABINOID RECEPTOR REGULATES IMMUNE-MEDIATED NEUROINFLAMMATION

Project description:Neuroinflammation is a recognized complication of immunotherapeutic approaches such as immune checkpoint inhibitor treatment, chimeric antigen receptor therapy, and graft versus host disease (GVHD) occurring after allogeneic hematopoietic stem cell transplantation. While T cells and inflammatory cytokines play a role in this process, the precise interplay between the adaptive and innate arms of the immune system that propagates inflammation in the central nervous system remains incompletely understood. Using a murine model of GVHD, we demonstrate that type 2 cannabinoid receptor (CB2R) signaling plays a critical role in the pathophysiology of neuroinflammation. In these studies, we identify that CB2R expression on microglial cells induces an activated inflammatory phenotype which potentiates the accumulation of donor-derived proinflammatory T cells, regulates chemokine gene regulatory networks, and promotes neuronal cell death. Pharmacological targeting of this receptor with a brain penetrant CB2R inverse agonist/antagonist selectively reduced neuroinflammation without deleteriously affecting systemic GVHD severity. Thus, these findings delineate a therapeutically targetable neuroinflammatory pathway and has implications for the attenuation of neurotoxicity after GVHD and potentially other T cell-based immunotherapeutic approaches.

2024-05-13 | GSE252964 | GEO

Cannabinoid Receptor 1 Dependent Effects of Isopropoyl dodeycl fluorophosphonate on Hepatic Gene Expression

Project description:We tested the effects of isopropoyl dodecyl fluorophosphonate (IDFP) (10 mg/kg, i.p.), a pharmacological inhibitor of endocannabinoid degradation, on hepatic gene expression in mice. To determine if increased cannabinoid receptor 1 signaling is responsible for IDFP induced effects a subset of mice were pretreated with the cannabinoid receptor 1 antagonist (AM251) (10 mg/kg, i.p.). Total RNA obtained from liver of mice treated with DMSO (n=6), IDFP (n=8), or AM251/IDFP (n=5) (all 10 mg/kg i.p.) for 4 hours.

2011-09-30 | E-GEOD-22949 | biostudies-arrayexpress

Cannabinoid Receptor 1 Dependent Effects of Isopropoyl dodeycl fluorophosphonate on Hepatic Gene Expression

2011-10-01 | GSE22949 | GEO

Microglial cannabinoid receptor type 1 mediates social memory deficits produced by adolescent THC exposure and 16p11.2 duplication

Project description:Microglial cannabinoid receptor type 1 mediates social memory deficits produced by adolescent THC exposure and 16p11.2 duplication

| PRJNA1015239 | ENA

Role of myeloid cannabinoid CB1 receptor in atherosclerosis

Project description:Role of myeloid cannabinoid CB1 receptor in atherosclerosis

| PRJNA1049407 | ENA

Cannabinoid receptor type 2 expression in mouse brain: from mapping to regulation in microglia under inflammatory conditions [snRNA-seq]

Project description:Since its detection in the brain, the cannabinoid receptor type 2 (CB2) has been considered a promising therapeutic target for various neurological and psychiatric disorders. However, precise brain mapping of its expression is still lacking. Using magnetic cell sorting, calibrated RT-qPCR and single-nucleus RNAseq, we show that CB2 is expressed at a low level in all brain regions studied, mainly by few microglial cells, and by neurons in an even lower proportion. Upon lipopolysaccharide stimulation, modeling neuroinflammation in non-sterile conditions, we demonstrate that the inflammatory response is associated with a transient reduction in CB2 mRNA levels in brain tissue, particularly in microglial cells. This result, confirmed in the BV2 microglial cell line, contrasts with the positive correlation observed between CB2 mRNA levels and the inflammatory response upon stimulation by interferon-gamma, modeling neuroinflammation in sterile condition. Discrete brain CB2 expression might thus be up- or down-regulated depending on the inflammatory context.

2024-08-25 | GSE247268 | GEO

Cannabinoid receptor double knockout mice (Cnr1 -/- /Cnr2 -/-) in CHS model

Project description:We evaluated cutaneous contact hypersensitivity (CHS) in Cnr1-/-/Cnr2-/- animals using the obligate contact allergen 2,4-dinitrofluorobenzene (DNFB), which generates a specific cutaneous T-cell mediated allergic response upon repeated allergen contact. Allergic contact dermatitis affects about 5% of men and 11% of women in industrialized countries and is one of the leading causes for occupational diseases. In an animal model for cutaneous contact hypersensitivity we show that mice lacking both known cannabinoid receptors display exacerbated allergic inflammation. In contrast, fatty acid amide hydrolase deficient mice, which have increased levels of the endocannabinoid anandamide, displayed reduced allergic responses in the skin. Cannabinoid receptor antagonists exacerbated whereas receptor agonists attenuated allergic inflammation. These results demonstrate a protective role of the endocannabinoid system in contact allergy in the skin, and suggest a novel target for therapeutic intervention. Keywords: Strain (Wt versus Ko) and disease state (DNFB treated versus control).

2007-06-11 | GSE7694 | GEO

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