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Gut microbiota dysbiosis-mediated ceramides elevation contributes to corticosterone-induced depression by impairing mitochondrial function

ABSTRACT: Gut microbiota dysbiosis-mediated ceramides elevation contributes to corticosterone-induced depression by impairing mitochondrial function

PROVIDER: PRJNA953619 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24111118_1.fastq.gz	Fastqsanger.gz
	SRR24111118_2.fastq.gz	Fastqsanger.gz
	SRR24111119_1.fastq.gz	Fastqsanger.gz
	SRR24111119_2.fastq.gz	Fastqsanger.gz
	SRR24111120_1.fastq.gz	Fastqsanger.gz

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Gut microbiota dysbiosis-mediated ceramides elevation contributes to corticosterone-induced depression by impairing mitochondrial function

Project description:Background: As a worldwide threat to mental health, depression affects about 322 million people globally. Recently, the role of gut microbiota dysbiosis on the pathogenesis of depression has received widespread attention, but the underlying mechanism remains elusive.Results: Corticosterone (CORT)-treated mice showed depressive-like behaviors, a reduction in hippocampal neurogenesis, and an altered composition of gut microbiota (GM). Fecal microbial transplantation (FMT) from CORT-treated mice transferred depressive-like phenotypes and their dominant GM, especially bifidobacterium and lactobacillus, to the recipients. Fecal metabolic profiling showed that the relative abundances of fecal ceramides were significantly increased in CORT-treated and the recipient mice. Metagenomic sequencing exposed that bifidobacterium and lactobacillus might be responsible for gut ceramides production in CORT-treated mice. We then found that treatment with ceramides via oral gavage was sufficient to recapitulate the depressive-like phenotypes in wild -type mice. Finally, RNA-sequencing data exposed that most of the differentially expressed genes (DEGs) between ceramides-treated mice and the control group were enriched in oxidative phosphorylation (OXPHOS) pathway. Conclusion: We conclude that chronic exposure to CORT leads to an altered GM composition and consequent ceramides production, thus leading to subtle mitochondrial OXPHOS dysfunction in hippocampus, which may contribute to the development of depressive disorders.

2024-04-01 | GSE229237 | GEO

Project description:Gut microbiota dysbiosis-mediated ceramides elevation contributes to corticosterone-induced depression by impairing mitochondrial function

| PRJNA951946 | ENA

Project description:Gut microbiota dysbiosis mediated ceramides elevation contributes to corticosterone-induced depression by impairing mitochondrial function

| PRJNA951794 | ENA

Transcription profiling of rat brain cortex from corticosterone treated animals

Project description:Animal models represent a very useful tool for the study of depressive-like behaviour and for the evaluation of the therapeutic efficacy of antidepressants. Nevertheless, gene expression patterns of these different animal models and whether genes classically associated to human major depression are present in these genetic profiles remain unknown. Gene expression was evaluated in an animal model of depression: corticosterone-treated rats. Gene expression analyses were carried out using the AffymetrixÂ® GeneChipÂ® technology. Experiment Overall Design: In total, 19 animals were studied, 10 corticosterone-treated rats and 9 control rats

2008-06-16 | E-GEOD-9797 | biostudies-arrayexpress

Inflammatory Signatures of Microglia in the Mouse Model of Corticosterone-Induced Depression

Project description:Microglia-mediated inflammation has been recognized as a key feature of major depressive disorder. Although hypercortisolemia is commonly observed in depressed patients and can be predictive of treatment response, how such chronic exposure to this stress hormone may influence microglia is incompletely characterized. Here, we exploited a standard mouse model of depressive-like behaviors induced by repeated peripheral administration of corticosterone. Microglia in the prefrontal cortex of mice were profiled by bulk RNA sequencing, which exhibited increased expression of inflammatory markers. In addition, single-cell RNA sequencing further identified distinct molecular patterns of microglial responses. Moreover, we revealed the up-regulation of Pu.1 and Irf8, the two central transcription factors governing microglia-mediated inflammation, in the prefrontal cortex and hippocampus of corticosterone-treated mice, which similarly occurred in depressed patients' microglia. These results have established the inflammatory signatures of microglia in the mouse model recapitulating hypercortisolemia-related depression, providing new insights into developing diagnostic and therapeutic strategies.

2024-10-01 | GSE274360 | GEO

Inflammatory Signatures of Microglia in the Mouse Model of Corticosterone-Induced Depression

Project description:Inflammatory Signatures of Microglia in the Mouse Model of Corticosterone-Induced Depression

| PRJNA1146043 | ENA

Gene expression analysis of brain cortex of corticosterone-treated rats

Project description:Animal models represent a very useful tool for the study of depressive-like behaviour and for the evaluation of the therapeutic efficacy of antidepressants. Nevertheless, gene expression patterns of these different animal models and whether genes classically associated to human major depression are present in these genetic profiles remain unknown. Gene expression was evaluated in an animal model of depression: corticosterone-treated rats. Gene expression analyses were carried out using the Affymetrix® GeneChip® technology. Keywords: Treatment vs control comparative genomics study

2007-12-12 | GSE9797 | GEO

The hippocampal response to acute corticosterone elevation is altered in a mouse model for Angelman syndrome

Project description:Angelman Syndrome (AS) is a severe neurodevelopmental disorder, caused by the neuronal absence of the ubiquitin protein ligase E3A (UBE3A). UBE3A promotes ubiquitin-mediated protein degradation and functions as a transcriptional coregulator of nuclear hormone receptors, including the glucocorticoid receptor (GR). Previous studies showed anxiety-like behavior and hippocampal-dependent memory disturbances in AS mouse models. Hippocampal GR is an important regulator of the stress response and memory formation, and we therefore investigated whether the absence of UBE3A in AS mice disrupted GR signaling in the hippocampus. We first established a strong cortisol-dependent interaction between the GR ligand binding domain and a UBE3A nuclear receptor box in a high-throughput interaction screen. In vivo, we found that UBE3A-deficient AS mice displayed significantly more variation in circulating corticosterone levels throughout the day compared to wildtypes (WT), with low to undetectable levels of corticosterone at the trough of the circadian cycle. Additionally, we observed an enhanced transcriptomic response in the AS hippocampus following acute corticosterone treatment. Surprisingly, chronic corticosterone treatment showed less contrast between AS and WT mice in the hippocampus and liver transcriptomic responses. This suggests that UBE3A limits the acute stimulation of GR signaling, likely as a member of the GR transcriptional complex. Altogether, these data indicate that AS mice are more sensitive to acute glucocorticoid exposure in the brain compared to WT mice. This suggests that stress responsiveness is altered in AS which could lead to anxiety symptoms.

2022-12-23 | GSE221378 | GEO

The hippocampal response to acute corticosterone elevation is altered in a mouse model for Angelman syndrome

Project description:The hippocampal response to acute corticosterone elevation is altered in a mouse model for Angelman syndrome

| PRJNA914211 | ENA

Corticosterone regulation of mRNAs and and corresponding RU486 antagonism in astrocytes in vitro

Project description:Analysis of mRNA gene expression changes mediated by natural glucocorticoid ligand corticosterone in mouse cortical primary astrocyte cultures; also, parallel analysis of RU486 (mifepristone) antagonism of corticosterone-mediated mRNA changes. Total RNA obtained from astrocyte cultures subjected to 2, 4, or 6 hours of (1) 100nM corticosterone alone, (2) 500nM RU486 alone, or (3) 100nM corticosterone + 500nM RU486 exposure compared to vehicle control astrocyte cultures.

2013-01-09 | E-GEOD-39270 | biostudies-arrayexpress

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