Dataset Information


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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Steve Cole 

PROVIDER: E-GEOD-47153 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via β-adrenergic induction of myelopoiesis.

Powell Nicole D ND   Sloan Erica K EK   Bailey Michael T MT   Arevalo Jesusa M G JM   Miller Gregory E GE   Chen Edith E   Kobor Michael S MS   Reader Brenda F BF   Sheridan John F JF   Cole Steven W SW  

Proceedings of the National Academy of Sciences of the United States of America 20130923 41

Across a variety of adverse life circumstances, such as social isolation and low socioeconomic status, mammalian immune cells have been found to show a conserved transcriptional response to adversity (CTRA) involving increased expression of proinflammatory genes. The present study examines whether such effects might stem in part from the selective up-regulation of a subpopulation of immature proinflammatory monocytes (Ly-6c(high) in mice, CD16(-) in humans) within the circulating leukocyte pool.  ...[more]

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