Selenoprotein K deficiency-induced apoptosis: A role for calpain and the ERS pathway

Redox Biology

Xin-Wen Xu¹  Yu-Bin Chen²  Qiong Liu³  Shi-Zheng Jia³  Shao-Ling Huang³  Guo-Li Song³  Zhong-Hao Zhang³  Peter R. Hoffmann³  Chen Chen³ 

[1] Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen University, Shenzhen, China;Shenzhen Bay Laboratory, Shenzhen, China;Shenzhen Key Laboratory of Marine Bioresources and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, China;

关键词: SELENOK;    Calpain;    Endoplasmic reticulum stress;    Neuronal apoptosis;   

DOI  :  

来源: DOAJ

【 摘 要 】

Selenoprotein K (SELENOK), an endoplasmic reticulum (ER) resident protein, is regulated by dietary selenium and expressed at a relatively high level in neurons. SELENOK has been shown to participate in oxidation resistance, calcium (Ca2+) flux regulation, and the ER-associated degradation (ERAD) pathway in immune cells. However, its role in neurons has not been elucidated. Here, we demonstrated that SELENOK gene knockout markedly enhanced ER stress (ERS) and increased apoptosis in neurons. SELENOK gene knockout elicited intracellular Ca2+ flux and activated the m-calpain/caspase-12 cascade, thus inducing neuronal apoptosis both in vivo and in vitro. In addition, SELENOK knockout significantly reduced cognitive ability and increased anxiety in 7-month-old mice. Our findings reveal an unexpected role of SELENOK in regulating ERS-induced neuronal apoptosis.

【 授权许可】

Unknown