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

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. <i>In vitro</i>, 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. <i>In vitro</i>, 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.