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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

ORGANISM(S): Mus musculus

PROVIDER: GSE47153 | GEO | 2013/11/04

SECONDARY ACCESSION(S): PRJNA204592

REPOSITORIES: GEO

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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

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

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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.

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Genome-wide analysis of the effects of propranolol on angiosarcoma tumor cells

Project description:Analysis of the effects of 4 hr and 24 hr propranolol treatment on gene expression of SVR mouse angiosarcoma cells. The hypothesis tested in the present study was that inhibiton of beta adrenergic receptor signaling could ablate the oncogenic properties of angiosarcoma cells. Results provide important information of the response of angiosarcoma cells to ablated beta adrenergic receptor signaling. The total RNA was obtained from mouse angiosarcoma cells cultured in monolayer at 0, 4, and 24 hrs of 50 micromolar propranolol treatment. Illumina microarrays were performed to determine the whole genome expression changes following treatment.

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Propranolol inhibit tumor growth through reducing T cell exhaustion

Project description:Recently, targeting or reinvigorating exhausted T cells have become the focus of cancer immunotherapy. Propranolol, a non-selection β1 and β2 adrenergic receptor blocker, or in combination with other drug, can inhibit the development of various tumors. Additionally, β2-adrenergic receptor (ADRB2) signaling suppresses the effector function of CD8+ T cell. However, whether propranolol plays an anti-tumor role by directly inhibiting T cell exhaustion remains unclear. In this study, we found that Propranolol significantly inhibited the development of AOM/DSS-induced colorectal cancer, and reduced the exhaustion of infiltrating T cell in colorectal cancer tissues. The anti-tumor effect of propranolol was further determined by CT26, B16F10, and MC38 subcutaneous tumor models in vivo. Cell viability analysis showed that Propranolol concentration below 40 μM had no effect on the viability of CT26 colorectal cancer cells. We also found that propranolol treatment did not inhibit the growth of tumors in BALB/c nude mice. The above results indicated that Propranolol relied on T cells to exert its anti-tumor effects. Bioinformatics analysis highlighted that ADRB2 was positive correlated with T cell exhaustion signature in colon adenocarcinoma, pancreatic adenocarcinoma, testicular germ cell tumors, and glioblastoma multiforme patients using the website of GEPIA. Accordingly, Propranolol directly inhibited T cells exhaustion, and increased IFN-γ secretion of CD4+ and CD8+ T cells in vitro. Collectively, propranolol plays anti-tumor role by directly inhibiting T cell exhaustion.

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