Yongmin Xiong
Director of the Endemic Institute of Xi'an Jiaotong University, China
Title: The Study on GPX3 DNA Methylation for the Cartilage Damage Mechanism in Kashin-Beck Disease
Biography
Biography: Yongmin Xiong
Abstract
Kashin-Beck disease (KBD) is an endemic and disabling osteoarthropathy. Epidemiological investigations have shown that selenium deficiency may contribute to the etiopathogenesis of KBD, however, the mechanisms of Se deficient in cartilage damage of KBD are still not clear. Glutathione peroxidases3 (GPX3), a member of selenoproteins, is found to paly a crucial role in protecting against oxidative damage in human body. The aim of the study was to investigate the effects of GPX3 DNA methylation on cartilage damage. GPX3 methylation were detected in whole blood of KBD patients and chondrocytes by methylation-specific polymerase chain reaction. The GPX3 mRNA were measured in whole blood of KBD patients and chondrocyte by qRT-PCR. The expression of PI3K/Akt/c-fos signaling molecules in whole blood of KBD patients and chondrocytes using Western blotting. The results showed that the frequency of GPX3 methylation significantly was increased and GPX3 mRNA was decreased in KBD patients than that of controls, and protein expression of Gβγ, PI3Kp110, pAkt and c-fos in KBD group were up-regulated. In the cell experiments, the rates of cell apoptosis and GPX3 methylation were increased, and GPX3 mRNA was decreased and PI3K/Akt/c-fos expression were up-regulated in injured group using tert-Butyl hydroperoxide. However, The rates of apoptosis and GPX3 methylation were decreased, GPX3 mRNA was increased and PI3K/Akt/c-fos signaling pathway were down-regulated in three Se pre-protection groups, suggesting that aberrant DNA methylation of GPX3 might be one of cartilage damage mechanisms in KBD (This research were supported by National Natural Science Foundation in China No.81573104, 81773372).