Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression analysis of mouse BNST and blood cells after chronic social defeat stress (CSDS)

ABSTRACT: Chronic psychosocial stress is a risk factor for psychiatric disorders, and genetic factors interact in conferring susceptibility. The chronic social defeat stress (CSDS) mouse model allows identifying factors underlying resilience and susceptibility to chronic psychosocial stress. Following 10 days of CSDS, we collected the brain and blood tissues. We performed (1) AGO2 RNA immunoprecipitation-sequencing (AGO2 RIP-seq) of active miRNAs and their mRNA targets in the BNST. Additionally, we carried out RNA-seq and miRNA-seq from blood cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE122840 | GEO | 2019/08/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression analysis of mouse brain regions after chronic social defeat stress (CSDS)

Project description:Chronic psychosocial stress is a risk factor for psychiatric disorders, and genetic factors interact in conferring susceptibility. The chronic social defeat stress (CSDS) mouse model allows identifying factors underlying resilience and susceptibility to chronic psychosocial stress. We used RNA-sequencing to identify genes and pathways affected by CSDS in three brain regions: medial prefrontal cortex (mPFC), ventral hippocampus (vHPC), and bed nucleus of the stria terminalis (BNST), of male mice from strains C57BL/6Crl and DBA/2Crl.

2018-07-04 | GSE109315 | GEO

Gene expression analysis of mouse BNST and blood cells after chronic social defeat stress (CSDS)

Project description:Gene expression analysis of mouse BNST and blood cells after chronic social defeat stress (CSDS)

| PRJNA506950 | ENA

Gender specific transcription regulation in the prefrontal cortex following social defeat stress

Project description:Major depressive disorder (MDD) affects ~20% of the world population and is characterized by strong sexual dimorphism with females being 2-3 times more likely to develop this disorder. Previously, we demonstrated that a combination therapy with dihydrocaffeic acid (DHCA) and malvidin-glucoside (Mal-gluc) to synergistically target peripheral inflammation and stress-induced synaptic maladaptation in the brain was effective in alleviating chronic social defeat stress (CSDS)-induced depression-like phenotype in male mice. Here, we test the combination therapy in a female CSDS model for depression and compared sex-specific responses to stress in the periphery and the central nervous system. Similar to male mice, the combination treatment is also effective in promoting resilience against the CSDS-induced depression-like behavior in female mice. However, there are sex-specific differences in peripheral immune responses and differential gene regulation in the prefrontal cortex to chronic stress and to the treatment. These data indicate that while therapeutic approaches to combat stress-related disorders may be effective in both sexes, the mechanisms underlying these effects differ, emphasizing the need for inclusion of both sexes in preclinical studies using animal models.

2020-03-12 | GSE146845 | GEO

Proteomics on dmPFC of chronic social defeat stress (CSDS) mice

Project description:We utilized the chronic social-defeat stress model (CSDS) to induce depressive-like phenotypes in mice . An unbiased quantitative proteomic screening was conducted on the dmPFC, a critical brain region for depression pathogenesis.

2022-12-06 | PXD037878 |

Small RNA Sequencing of mouse prefrontal cortex after chronic social defeat stress (CSDS)

Project description:Small RNA Sequencing of mouse prefrontal cortex after chronic social defeat stress (CSDS)

| PRJNA491729 | ENA

Gene expression analysis of mouse brain regions after chronic social defeat stress (CSDS)

Project description:Gene expression analysis of mouse brain regions after chronic social defeat stress (CSDS)

| PRJNA430409 | ENA

iTRAQ-based proteomics suggests Ephb6 as a potential regulator of the ERK pathway in the prefrontal cortex of chronic social defeat stress model miceiTRAQ-based proteomics reveals Ephb6 as a potential regulator of the ERK pathway in the prefrontal cortex of chronic social defeat stress model mice

Project description:Purpose: Major depressive disorder (MDD) is a worldwide concern and devastating psychiatric disease. The World Health Organization claims that MDD leads to at least 11.9% of the global burden of disease. However, the underlying pathophysiology mechanisms of MDD remain largely unknown. Experimental design: Herein, we used a proteomic-based strategy to compare the prefrontal cortex (PFC) in chronic social defeat stress (CSDS) model mice with a control group. Based on pooled samples, differential proteins were identified in the PFC proteome using iTRAQ coupled with LC-MS/MS. Results: Ingenuity Pathway Analysis (IPA) was then followed to predict relevant pathways, with the ephrin receptor signaling pathway selected for further research. Additionally, as the selected key proteins of the ephrin receptor signaling pathway, ephrin type-B receptor 6 (EphB6) and the ERK pathway were validated by western blotting. Conclusion and clinical relevant: Altogether, increased understanding of the ephrin receptor signaling pathway in MDD is provided, which implicates further investigation of PFC dysfunction induced by CSDS treatment.

2018-07-05 | PXD007573 | Pride

H3K79me2 dynamics in medium spiny neurons mediate long-term behavioral and cell type-specific molecular effects of early life stress

Project description:Animals susceptible to chronic social defeat stress (CSDS) exhibit depression-related behaviors, and show aberrant transcription across several limbic brain regions. The nucleus accumbens (NAc) in particular shows unique susceptible versus resilient phenotypes at the transcriptional, neuroanatomical, and physiological levels. Early life stress (ELS) promotes susceptibility to CSDS in adulthood, but associated enduring changes in transcriptional control mechanisms in NAc have not yet been investigated. Here, we examined long-lasting changes in histone modifications induced in NAc by ELS and studied their underlying mechanisms in mediating heightened lifelong stress susceptibility in male and female mice. We identify methylation of lysine 79 of histone H3 (H3K79me) and the enzymes that control this modification, selectively in D2-type medium spiny neurons, as crucial for the expression of ELS-induced stress susceptibility, and reveal the transcriptional networks regulated by this mechanism. Finally, we demonstrate the potential clinical viability of this approach by showing that systemic delivery of a small molecule inhibitor of H3K79me reverses ELS-induced behavioral deficits.

2020-12-09 | GSE133889 | GEO

Myelin-Associated Oligodendrocytic Basic Protein-Dependent Myelin Repair Confers the Long-lasting Antidepressant Effect of Ketamine

Project description:To examine ketamine’s long-lasting effects on gene expression in the brains of mice exhibiting depression-like behaviors, we used spatial transcriptomics (ST) to analyze transcriptomics on the cortices of mice exposed to chronic social defeat stress (CSDS) and treated with ketamine.

2023-10-12 | GSE214861 | GEO

Circuit-wide transcriptional profiling reveals region specific gene co-expression networks regulating depression susceptibility

Project description:Depression is a complex and heterogeneous disorder and a leading contributor to the global burden of of disease. Most previous research has focused on individual brain regions and individual genes that contribute to depression. However, emerging evidence in both humans and animal models suggests that dysregulated circuit function and gene expression across multiple brain regions drive depressive phenotypes. Here we use a bioinformatics approach intersecting differential expression analysis with weighted gene co-expression network analysis to identify transcriptional networks that regulate susceptibility to depressive-like symptoms in mice. We performed RNA-sequencing on multiple brain regions from control animals and those either susceptible or resilient to chronic social defeat stress (CSDS) at multiple time points after defeat. We bioinformatically identified several transcriptional networks that regulate depression susceptibility, and in vivo manipulations of these networks confirmed their functional significance at the levels of gene transcription, synaptic regulation, and behavior. Our findings reveal novel transcriptional networks that control stress susceptibility and offer fundamentally new leads for antidepressant drug discovery.

2016-05-12 | GSE72343 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data