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

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

PROVIDER: PRJNA430409 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6498960.fastq.gz	Fastqsanger.gz
	SRR6498970.fastq.gz	Fastqsanger.gz
	SRR6498980.fastq.gz	Fastqsanger.gz
	SRR6498990.fastq.gz	Fastqsanger.gz
	SRR6499000.fastq.gz	Fastqsanger.gz

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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.

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Gene expression analysis of mouse BNST and blood cells 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. 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.

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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)

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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)

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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.

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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.

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Project description:Susceptibility to depression-like behavioral abnormalities in mice is studied with a well-established social defeat stress model. Responses to social defeat are associated with widespread transcriptomic changes in several brain regions. Here we present the first study of genome-wide cytosine methylation patterns of mice susceptible to social defeat stress using whole-genome bisulfite sequencing on DNA from the nucleus accumbens, a key brain reward region implicated in depression. We find a greater proportion of CpG hypermethylation than hypomethylation in susceptible mice compared to controls, with an opposite trend in the CHG and CHH contexts. Among the genes with the largest extent of differential methylation we find several which have been identified in earlier studies of gene expression changes related to social defeat, including estrogen receptor alpha (encoded by Esr1) and the deleted in colorectal cancer (Dcc) gene. Genes exhibiting differential methylation are enriched in GO terms of nervous system development, neurogenesis and structure development, which associated with learning memory and stress response. Our data provide a new evidence of the association of DNA methylation profiles and susceptibility to chronic stress.

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