Rongqiang Zhang1,2, Hao Guo2, Xiaoli Yang2, Dandan Zhang2, Di Zhang2, Qiang Li2, Chen Wang2, Xuena Yang2, Yongmin Xiong2. 1. School of Public Health, Shaanxi University of Chinese Medicine, Xianyang, China. 2. Institute of Key Laboratory of Trace Elements and Endemic Diseases, National Health Commission of the People's Republic of China, School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
Abstract
OBJECTIVE: We aimed to analyze deoxycytidine-deoxyguanosine dinucleotide (CpGs) methylation profiles in DIO2, GPX3, and TXNRD1 promoter regions in osteoarthritis (OA) and Kashin-Beck disease (KBD) patients. METHODS: Blood samples were collected from 16 primary OA patients and corresponding 16 healthy individuals and analyzed for methylations in the CpGs of DIO2, GPX3, and TXNRD1 promoter regions using MALDI-TOF-MS. The methylation profiles of these regions were then compared between OA and KBD patients. RESULTS: DIO2-1_CpG_2 and DIO2-1_CpG_3 methylations were significantly lower in OA than KBD patients (P < 0.05). A similar trend was observed for GPX3-1_CpG_4, GPX3-1_CpG_7, GPX3-1_CpG_8.9.10, GPX3-1_CpG_13.14.15 and GPX3-1_CpG_16 (P < 0.05) as well as TXNRD1-1_CpG_1 and TXNRD1-1_CpG_2 methylation between OA and KBD patients (P < 0.05). However, there was no difference in methylation levels of other CpGs between the 2 groups (P > 0.05). CONCLUSION: OA and KBD patients display distinct methylation profiles in the CpG sites of DIO2, GPX3, and TXNRD1 promoter regions. These findings provide a strong background and new perspective for future studies on mechanisms underlying epigenetic regulation of selenoprotein genes associated with OA and KBD diseases.
OBJECTIVE: We aimed to analyze deoxycytidine-deoxyguanosine dinucleotide (CpGs) methylation profiles in DIO2, GPX3, and TXNRD1 promoter regions in osteoarthritis (OA) and Kashin-Beck disease (KBD) patients. METHODS: Blood samples were collected from 16 primary OA patients and corresponding 16 healthy individuals and analyzed for methylations in the CpGs of DIO2, GPX3, and TXNRD1 promoter regions using MALDI-TOF-MS. The methylation profiles of these regions were then compared between OA and KBD patients. RESULTS: DIO2-1_CpG_2 and DIO2-1_CpG_3 methylations were significantly lower in OA than KBD patients (P < 0.05). A similar trend was observed for GPX3-1_CpG_4, GPX3-1_CpG_7, GPX3-1_CpG_8.9.10, GPX3-1_CpG_13.14.15 and GPX3-1_CpG_16 (P < 0.05) as well as TXNRD1-1_CpG_1 and TXNRD1-1_CpG_2 methylation between OA and KBD patients (P < 0.05). However, there was no difference in methylation levels of other CpGs between the 2 groups (P > 0.05). CONCLUSION: OA and KBD patients display distinct methylation profiles in the CpG sites of DIO2, GPX3, and TXNRD1 promoter regions. These findings provide a strong background and new perspective for future studies on mechanisms underlying epigenetic regulation of selenoprotein genes associated with OA and KBD diseases.
Entities:
Keywords:
CpG; CpG-SNP; DNA methylation; Kashin-Beck disease; osteoarthritis
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