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Microglial RNA-sequencing after stress-sensitization by repeated social defeat

ABSTRACT: Microglial RNA-sequencing after stress-sensitization by repeated social defeat

PROVIDER: PRJNA510940 | ENA |

REPOSITORIES: ENA

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Microglial RNA-sequencing after stress-sensitization by repeated social defeat

Project description:Stress is associated with an increased prevalence of anxiety and depression. Repeated social defeat (RSD) stress in mice increases the release of monocytes from the bone marrow that are recruited to the brain by microglia. These monocytes enhance inflammatory signaling and augment anxiety. Moreover, RSD promotes stress sensitization, in which exposure to acute stress 24 days after cessation of RSD causes anxiety recurrence. The purpose of this study was to determine whether microglia were critical to stress sensitization and exhibited altered gene expression 24 days after RSD.

2018-12-21 | GSE124169 | GEO

Gene expression alteration in the hippocampus of depression mouse model with repeated social defeat stress

Project description:We used microarrays to identify the gene with altered expression in the hippocampus of depression mouse model with repeated social defeat stress campared to control mice.

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Differential gene expression in peripheral blood leukocytes from mice subject to repeated social defeat

Project description:This study tested the effects of repeated social defeat (RSD) on gene expression in peripheral blood mononuclear cells (PBMC), and examined the extent to which these effects were abrogated by depletion of CD11b+ cells (monocytes). Study Type: Risk prediction Gene expression profiling was carried out on peripheral blood mononuclear cell (PBMC) mRNA samples collected from 18 mice randomized to either 6 cycles of repeated social defeat (RSD, n=9) or to home cage control (HCC, n=9) conditions. PBMC samples were pooled into 3 groups of n=3 samples in each condition, and Illumina Mouse Ref-8 BeadArray assays were performed on approximately 1 million total PBMC and 1 million PBMC from which CD11b+ cells were immunomagnetically depleted by MACS. The primary research questions are 1) whether expression of pro-inflammatory genes is altered by RSD, and 2) whether depletion of CD11b+ cells (monocytes) abrogates these effects.

2013-11-04 | E-GEOD-47154 | biostudies-arrayexpress

Differential gene expression in peripheral blood leukocytes from mice subject to repeated social defeat

2013-11-04 | GSE47154 | GEO

The effect of Repeated Social defeat stress (RSD) on transcriptomic profiles of rat heart

Project description:This study investigated risk factors that may contribute to stress-related cardiac disease susceptibility and progression in a rodent model. The experiment was designed to evaluate the transcriptomic changes in in the heart of male adult rats after repeated episodes of social defeat stress.

2021-03-19 | GSE169181 | GEO

Effect of propranolol on differential gene expression in peripheral blood monocytes from mice subject to repeated social defeat

2013-11-04 | GSE47153 | GEO

Effect of propranolol on differential gene expression in peripheral blood monocytes from mice subject to repeated social defeat

Project description:This study tested the effects of repeated social defeat (RSD) on gene expression in peripheral blood monocytes and examined the extent to which these effects were abrogated by the beta-adrenergic antagonist propranolol. Study Type: Risk prediction Gene expression profiling was carried out on peripheral blood monocyte mRNA samples collected from 36 mice randomized to either 6 cycles of repeated social defeat (RSD, n=18) or to parallel home cage control (HCC, n=18) conditions. Within each condition (RSD vs HCC), 9 animals were treated with the beta-adrenergic antagonist propranolol and 9 were treated with an equivalent volume of vehicle. After 6 cycles of RSD or parallel HCC, blood samples were pooled into groups of n=3 samples in each condition, and Illumina Mouse Ref-8 BeadArray assays were performed on RNA from approximately 1 million CD11b+ peripheral blood mononuclear cells (i.e., monocytes) which were immunomagnetically isolated by MACS. The primary research questions are 1) whether expression of pro-inflammatory genes is altered by RSD, and 2) whether treatment with propranolol abrogates these effects.

2013-11-04 | E-GEOD-47153 | biostudies-arrayexpress

Gene expression profile at single cell level of splenocytes from wild-type and S100a9 knock-out mice ± repeated social defeat stress

Project description:Psychological trauma increases inflammation. In a mouse model of psychological trauma (repeated social defeat stress), we used single cell RNA sequencing to assess the gene expression in splenocytes ± psychological trauma as well as without S100a9 (gene of interest)

2023-01-01 | GSE209553 | GEO

Expression data from ileum of mice suffered from subchronic and mild social defeat stress

Project description:This study aimed to investigate the effects of depression on transcriptome in ileum using a subchronic and mild social defeat stress (sCSDS) model. In addition to exhibiting social deficit and hyperphagia-like behavior, the sCSDS mice keep much more water in their body than control mice. In order to investigate the effect of social defeat stress on not only central nervous system but also function of gastrointestinal tract, the gene expression in ileum of stressed mice was compared with control mice. We used microarrays to detail the gene expression after 10 days of social defeat stress and identified distinct classes of down-regulated genes during this process. The duration of physical contacts was set at 5 min after the first attack bite at Day 1, and then was reduced 0.5 min per day from Day 2 to Day 10.

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Social defeat effect on mice prefrontal cortex

Project description:Behavioral analysis confirmed that the 14-day social defeat sessions resulted in induction of depressive-like states measured in social interaction and light/dark tests. The combined data show that stress-induced depressive states are associated with molecular and structural changes that demyelinate the prefrontal cortex.

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