Down-regulation of microRNA-155 promotes selenium deficiency-induced apoptosis by tumor necrosis factor receptor superfamily member 1B in the broiler spleen
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Ci Liu1, Zhepeng Sun1, Zhe Xu1, Tianqi Liu1, Tingru Pan1 and Shu Li1
1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. China
Shu Li, email: email@example.com
Keywords: broiler, spleen, lymphocyte apoptosis, microRNA-155, tumor necrosis factor receptor superfamily member 1B
Received: February 03, 2017 Accepted: March 22, 2017 Published: April 19, 2017
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.
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