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Expression profiling of selenium deficiency in mouse colon and splenic leukocytes

ABSTRACT: Expression profiling of selenium deficiency in mouse colon and splenic leukocytes

PROVIDER: PRJNA480869 | ENA |

REPOSITORIES: ENA

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Marginal selenium deficiency down-regulates inflammation-related genes in splenic leukocytes of the mouse

Project description:Moderate selenium deficiency may lead to an impaired capacity to cope with health challenges. Functional effects of suboptimal selenium intake are not fully known, and biomarkers for an insufficient selenium supply are inadequate. We therefore fed mice diets of moderately deficient or adequate selenium intake for 6 weeks. Changes in global gene expression were monitored by microarray analysis in splenic leukocytes. Genes for four selenoproteins, Sepw1, Gpx1, Selh and Sep15, were the most significantly down-regulated in moderate selenium deficiency, and this was confirmed by quantitative polymerase chain reaction (qPCR). Classification of significantly affected genes revealed that processes related to inflammation, heme biosynthesis, DNA replication and transcription, cell cycle and transport were affected by selenium restriction. Down-regulation by moderate selenium deficiency of specific genes involved in inflammation and heme biosynthesis was confirmed by qPCR. Myeloperoxidase and lysozyme activities were decreased in selenium-restricted leukocytes, providing evidence for functional consequences. Genes for 31 nuclear factor (NF)-κB targets were down-regulated in moderate selenium deficiency, indicating an impaired NF-κB signaling. Together, the observed changes point to a disturbance in inflammatory response. The selenoproteins found here to be sensitive to selenium intake in murine leukocytes might also be useful as biomarkers for a moderate selenium deficiency in humans.

2018-07-13 | GSE117026 | GEO

Marginal selenium deficiency down-regulates inflammation-related genes in splenic leukocytes of the mouse

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Four selenoproteins, protein biosynthesis, and Wnt signalling are particularly sensitive to limited selenium intake in mouse colon

Project description:Selenium is an essential micronutrient. Its recommended daily allowance is not attained by a significant proportion of the population in many countries and its intake has been suggested to affect colorectal carcinogenesis. Therefore, microarrays were used to determine how both selenoprotein and global gene expression patterns in the mouse colon were affected by marginal selenium deficiency comparable to variations in human dietary intakes. Two groups of 12 mice each were fed a selenium-deficient (0.086mg Se/kg) or a selenium-adequate (0.15mg Se/kg) diet. After 6wk, plasma selenium level, liver, and colon glutathione peroxidase (GPx) activity in the deficient group was 12, 34, and 50%, respectively, of that of the adequate group. Differential gene expression was analysed with mouse 44K whole genome microarrays. Pathway analysis by GenMAPP identified the protein biosynthesis pathway as most significantly affected, followed by inflammation, Delta-Notch and Wnt pathways. Selected gene expression changes were confirmed by quantitative real-time PCR. GPx1 and the selenoproteins W, H, and M, responded significantly to selenium intake making them candidates as biomarkers for selenium status. Thus, feeding a marginal selenium-deficient diet resulted in distinct changes in global gene expression in the mouse colon. Modulation of cancer-related pathways may contribute to the higher susceptibility to colon carcinogenesis in low selenium status.

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Gene expression profile of isolated splenic NK cells from mice treated with ptaquiloside and/or selenium

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Expression profiling of selenium deficiency in mouse colon and splenic leukocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-07-13 | GSE117027 | GEO

Gene expression profile of isolated splenic NK cells from mice treated with ptaquiloside and/or selenium

Project description:To better understand the immunosuppressor mechanism of ptaquiloside in splenic NK cells and the reversion of this effect by selenium, we have employed whole genome microarray expression profile to identify genes associated with immunosuppression. Among 89 genes induced by ptaquiloside treatment in splenic NK cells only two genes (Mt1 and Mt2) were identified as related with its immunosuppressor effect. Moreover this augmented expression of Mt1 and Mt2 was totally abrogated by selenium co-treatment. These results were confirmed by flow cytometry in splenic cells harvested from other six mice and treated in vitro for 1 hour with ptaquiloside and/or selenium. Twenty mice were separated randomly into four groups as Control (water), Pt (ptaquiloside 5.3 mg/kg), PtSe (ptaquiloside 5.3 mg/kg and selenium 1.3 mg/kg) and Se (selenium 1.3 mg/kg) and were treated daily by gavage for 14 days. After treatment, untouched NK cells were isolated using the NK cell isolation kit, LS columns, and QuadroMACS cell separator system (Miltenyi Biotec, Inc.) to perform RNA isolation and whole-genome gene expression profile. Thereby, five independent experiments were performed per group using different donors for each experiment. To confirm the increase of metallothionein protein induced by ptaquiloside, splenic cells were harvested from other six mice and treated in vitro for 1 hour with ptaquiloside [4.4 M-BM-5g/mL] and/or selenium [0.1 mM] and analyzed by flow cytometry.

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