Down-regulation of microRNA-155 promotes selenium deficiency-induced apoptosis by tumor necrosis factor receptor superfamily member 1B in the broiler spleen.

Ci Liu,Zhe Xu,Tianqi Liu,Tingru Pan,Zhepeng Sun,Shu Li

doi:10.18632/oncotarget.17222

Ci Liu, Zhe Xu + Show 4 more

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https://doi.org/10.18632/oncotarget.17222

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Journal: Oncotarget	Publication Date: Apr 19, 2017
Citations: 12	License type: cc-by

Affiliation: Northeast Agricultural University

Abstract

The aim of this work was to explore the microRNA profile and the effect of microRNA-155 on apoptosis in the spleen of selenium-deficient broilers. We replicated the splenic-apoptotic model in selenium-deficient broilers. In vitro, microRNA-155 oligonucleotides were transfected into lymphocytes and subsequently treated with H2O2. We observed that selenium deficiency altered the microRNA profile and decreased the expression of microRNA-155 in the broiler spleens. Tumor necrosis factor receptor superfamily member 1B was verified as a target of microRNA-155 in the splenocytes. Morphological changes, increased levels of tumor necrosis factor receptor superfamily member 1B, c-Jun N-terminal kinase, Bak, Bax, Cyt-c, caspase9 and caspase3 and decreased levels of Bcl-2 demonstrated that selenium deficiency induced apoptosis in the spleen tissues. In vitro, microRNA-155 m inhibited the levels of ROS and reduced apoptosis compared with microRNA-155i in the lymphocytes. These results suggested that the reduced levels of microRNA-155 due to selenium deficiency could promote oxidative stress-induced apoptosis by increased tumor necrosis factor receptor superfamily member 1B in splenic cells.

Highlights

The essential trace mineral selenium is of fundamental importance in animal health
These results suggested that the reduced levels of microRNA-155 due to selenium deficiency could promote oxidative stress-induced apoptosis by increased tumor necrosis factor receptor superfamily member 1B in splenic cells
The expression of microRNA-155 in the L group was significantly reduced to ~43% (P < 0.05) compared with the C group. These results suggested that selenium deficiency altered the microRNA expression profile and reduced the expression of microRNA-155

Summary

Introduction

The essential trace mineral selenium is of fundamental importance in animal health. Selenium plays a crucial role in immunomodulation [1]. Selenium deficiency impaired the host innate immune response by inducing changes in the levels of cytokine expression in the spleens of mice [7]. Apoptosis linked to nitric oxide was induced by selenium deficiency in the immune organs of laying hens [12]. The selenium supply can alter the microRNA expression profile. Our aim was to investigate the effects of selenium deficiency on the microRNA profile and the mechanism of microRNAs in apoptosis of splenic cells. We found that selenium deficiency altered the microRNA profile and reduced the expression of microRNA-155 in the tissues of the spleen. Reduced levels of microRNA-155 promoted apoptosis by targeting TNFRSF1B in the spleen tissues of broilers suffering from selenium deficiency. This study explored the role of selenium deficiency in apoptosis to determine the signal transduction pathways involved, and the findings will help to elucidate the biological mechanisms in which selenium is involved

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