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Molecular mechanisms of cannabinoid type II receptor agonists in a mouse model of psychological stress-induced cardiac injury revealed by whole transcriptomic analysis

ABSTRACT: Molecular mechanisms of cannabinoid type II receptor agonists in a mouse model of psychological stress-induced cardiac injury revealed by whole transcriptomic analysis

PROVIDER: PRJNA867671 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20986909.fastq.gz	Fastqsanger.gz
	SRR20986910.fastq.gz	Fastqsanger.gz
	SRR20986911.fastq.gz	Fastqsanger.gz
	SRR20986912.fastq.gz	Fastqsanger.gz
	SRR20986913.fastq.gz	Fastqsanger.gz

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Molecular mechanisms of cannabinoid type II receptor agonists in a mouse model of psychological stress-induced cardiac injury revealed by whole transcriptomic analysis

Project description:To investigate the mechanisms of chronic psychological stress-induced cardiac injury and the protective mechanisms of cannabinoid type II agonists in a model of psychological stress-induced cardiac injury We constructed a mouse chronic psychological stress model based on a chronic unpredictable stress pattern. Mice were randomly divided into control, case (psychological stress group), and treatment groups (post-stress with the cannabinoid type II receptor agonist JWH133) to begin a 3-week psychological stress procedure, and cardiac tissue was subsequently removed for whole-transcriptome sequencing

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

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Transcription profiling of mouse Cannabinoid receptor double knockouts (Cnr1 -/- /Cnr2 -/-) in CHS model to investigate cutaneous contact hypersensitivity

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. Experiment Overall Design: Three wildtype mice (Wt) and three Cnr1-/-/Cnr2-/- (Ko) mice were used. Contact hypersensitivity was determined always at the right ears, which therefore were treated with DNFB (Tr). Left ears of mice were kept untreated and served as control ears (C). A total of 12 hybridizations were performed (2 strains x 2 treatments X 3 biological replicates) in this experiment.

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

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

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Leukocyte gene expression variation as a function of psychological well-being II

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Project description:Mental health profoundly impacts inflammatory responses in the body. This is particularly apparent in inflammatory bowel disease (IBD), where psychological stress is associated with disease flares. Here, we discover a critical role for the enteric nervous system (ENS) in mediating the aggravating effect of chronic stress on intestinal inflammation. We find that chronically elevated levels of glucocorticoids drive the generation of an inflammatory subset of enteric glia that promotes monocyte- and TNF-mediated colitis via CSF1. Additionally, glucocorticoids cause transcriptional immaturity in enteric neurons, acetylcholine deficiency, and dysmotility via TGFβ2. We verify the connection between the psychological state, intestinal inflammation, and dysmotility in two cohorts of human IBD patients. Together, these findings offer a mechanistic explanation for the impact of the brain on peripheral inflammation, define the ENS as a relay between psychological stress and gut inflammation, and suggest that stress management could serve as a valuable component of IBD care.

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