The study of GPX3 methylation in patients with Kashin-Beck Disease and its mechanism in chondrocyte apoptosis

Bone
LiXin HanYongMin Xiong

Abstract

Selenium deficiency is a risk factor for Kashin-Beck Disease (KBD), an endemic osteoarthropathy. Although promoter hypermethylation of glutathione peroxidase 3 (GPX3) (a selenoprotein) has been identified in several cancers, little is known about promoter methylation and expression of GPX3 and their relation to selenium in KBD. The present study was thus conducted to investigate this research question. Methylation and expressions of GPX3 in whole blood drawn from 288 KBD patients and 362 healthy controls and in chondrocyte cell line were evaluated using methylation-specific PCR and qRT-PCR, respectively. The protein levels of PI3K/Akt/c-fos signaling in the whole blood and chondrocyte cell line were determined with Western blotting. Chondrocytes apoptosis were detected by Hoechst 33342 and Annexin V-FITC/PI staining. GPX3 methylation was increased, GPX3 mRNA was decreased, and protein levels in the PI3K/Akt/c-fos signaling pathway were up-regulated in the whole blood collected from KBD patients as compared with healthy controls. Similar results were obtained for chondrocytes injured by oxidative stress. There was a significant, decreasing trend in GPX3 expression across groups of unmethylation, partial methylation, and complete...Continue Reading

Citations

May 28, 2020·Journal of Cellular Physiology·Zhaofang LiYongmin Xiong
Aug 13, 2020·Cancers·Caroline ChangNadine Hempel
Feb 23, 2021·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Jia XiaoshiZhao Ke

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