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.
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.
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
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
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.
Project description:Gene expression profiling was carried out on peripheral blood leukocytes from 14 healthy older adults. The primary research question is whether gene expression differs in individuals experiencing chronically high levels of social isolation (by UCLA Loneliness Scale) vs chronically low levels of social isolation. Experiment Overall Design: Gene expression profiling was carried out on peripheral blood leukocytes from 14 healthy older adults. The primary research question is whether gene expression differs in individuals experiencing chronically high levels of social isolation (by UCLA Loneliness Scale) vs chronically low levels of social isolation.
Project description:Gene expression profiling was carried out on splenocyte mRNA samples collected from 10 animals subject to repeated social threat (pooled into 2 groups of 5) and 10 animals subject to non-threatening control conditions (pooled into 2 groups of 5). The primary research question is whether gene expression differs in CD11b+ splenocytes from animals exposed to social threat vs non-threatening control conditions. Keywords: Risk prediction RNA from 5 mice/sample was pooled to generate 4 total samples: 2 from mice subject to repeated social threat, and 2 from control mice.
Project description:Gene expression profiling was carried out on prefrontal cortex mRNA samples collected from 10 animals subject to repeated social threat (pooled into 2 groups of 5) and 10 animals subject to non-threatening control conditions (pooled into 2 groups of 5). The primary research question is whether gene expression differs in prefrontal cortex tissue from animals exposed to social threat vs non-threatening control conditions. Keywords: Risk prediction RNA from 5 mice/sample was pooled to generate 4 total samples: 2 from mice subject to repeated social threat, and 2 from control mice.
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.
