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Integrating genome-wide DNA methylation and mRNA expression profiles identified different molecular features between Kashin-Beck disease and primary osteoarthritis.
Arthritis Res Ther. 2018 03 07; 20(1):41.AR

Abstract

BACKGROUND

Kashin-Beck disease (KBD) is an endemic osteochondropathy of unknown etiology. Osteoarthritis (OA) is a form of degenerative joint disease sharing similar clinical manifestations and pathological changes to articular cartilage with KBD.

METHODS

A genome-wide DNA methylation profile of articular cartilage from five KBD patients and five OA patients was first performed using the Illumina Infinium HumanMethylation450 BeadChip. Together with a previous gene expression profiling dataset comparing KBD cartilage with OA cartilage, an integrative pathway enrichment analysis of the genome-wide DNA methylation and the mRNA expression profiles conducted in articular cartilage was performed by InCroMAP software.

RESULTS

We identified 241 common genes altered in both the DNA methylation profile and the mRNA expression profile of articular cartilage of KBD versus OA, including CHST13 (NM_152889, fold-change = 0.5979, P methy = 0.0430), TGFBR1 (NM_004612, fold-change = 2.077, P methy = 0.0430), TGFBR2 (NM_001024847, fold-change = 1.543, P methy = 0.037), TGFBR3 (NM_001276, fold-change = 0.4515, P methy = 6.04 × 10-4), and ADAM12 (NM_021641, fold-change = 1.9768, P methy = 0.0178). Integrative pathway enrichment analysis identified 19 significant KEGG pathways, including mTOR signaling (P = 0.0301), glycosaminoglycan biosynthesis-chondroitin sulfate/dermatan sulfate (P = 0.0391), glycosaminoglycan biosynthesis-keratan sulfate (P = 0.0278), and PI3K-Akt signaling (P = 0.0243).

CONCLUSION

This study identified different molecular features between Kashin-Beck disease and primary osteoarthritis and provided novel clues for clarifying the pathogenetic differences between KBD and OA.

Authors+Show Affiliations

Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China. The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China. fzhxjtu@mail.xjtu.edu.cn.Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Xi'an Jiaotong University, Health Science Center, No.76 Yan Ta West Road, Xi'an, 710061, People's Republic of China. guox@mail.xjtu.edu.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29514696

Citation

Wen, Yan, et al. "Integrating Genome-wide DNA Methylation and mRNA Expression Profiles Identified Different Molecular Features Between Kashin-Beck Disease and Primary Osteoarthritis." Arthritis Research & Therapy, vol. 20, no. 1, 2018, p. 41.
Wen Y, Li P, Hao J, et al. Integrating genome-wide DNA methylation and mRNA expression profiles identified different molecular features between Kashin-Beck disease and primary osteoarthritis. Arthritis Res Ther. 2018;20(1):41.
Wen, Y., Li, P., Hao, J., Duan, C., Han, J., He, A., Du, Y., Liu, L., Liang, X., Zhang, F., & Guo, X. (2018). Integrating genome-wide DNA methylation and mRNA expression profiles identified different molecular features between Kashin-Beck disease and primary osteoarthritis. Arthritis Research & Therapy, 20(1), 41. https://doi.org/10.1186/s13075-018-1531-1
Wen Y, et al. Integrating Genome-wide DNA Methylation and mRNA Expression Profiles Identified Different Molecular Features Between Kashin-Beck Disease and Primary Osteoarthritis. Arthritis Res Ther. 2018 03 7;20(1):41. PubMed PMID: 29514696.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Integrating genome-wide DNA methylation and mRNA expression profiles identified different molecular features between Kashin-Beck disease and primary osteoarthritis. AU - Wen,Yan, AU - Li,Ping, AU - Hao,Jingcan, AU - Duan,Chen, AU - Han,Jing, AU - He,Awen, AU - Du,Yanan, AU - Liu,Li, AU - Liang,Xiao, AU - Zhang,Feng, AU - Guo,Xiong, Y1 - 2018/03/07/ PY - 2017/08/22/received PY - 2018/02/01/accepted PY - 2018/3/9/entrez PY - 2018/3/9/pubmed PY - 2019/5/15/medline KW - Gene expression KW - Kashin-Beck disease KW - Methylation KW - Osteoarthritis SP - 41 EP - 41 JF - Arthritis research & therapy JO - Arthritis Res. Ther. VL - 20 IS - 1 N2 - BACKGROUND: Kashin-Beck disease (KBD) is an endemic osteochondropathy of unknown etiology. Osteoarthritis (OA) is a form of degenerative joint disease sharing similar clinical manifestations and pathological changes to articular cartilage with KBD. METHODS: A genome-wide DNA methylation profile of articular cartilage from five KBD patients and five OA patients was first performed using the Illumina Infinium HumanMethylation450 BeadChip. Together with a previous gene expression profiling dataset comparing KBD cartilage with OA cartilage, an integrative pathway enrichment analysis of the genome-wide DNA methylation and the mRNA expression profiles conducted in articular cartilage was performed by InCroMAP software. RESULTS: We identified 241 common genes altered in both the DNA methylation profile and the mRNA expression profile of articular cartilage of KBD versus OA, including CHST13 (NM_152889, fold-change = 0.5979, P methy = 0.0430), TGFBR1 (NM_004612, fold-change = 2.077, P methy = 0.0430), TGFBR2 (NM_001024847, fold-change = 1.543, P methy = 0.037), TGFBR3 (NM_001276, fold-change = 0.4515, P methy = 6.04 × 10-4), and ADAM12 (NM_021641, fold-change = 1.9768, P methy = 0.0178). Integrative pathway enrichment analysis identified 19 significant KEGG pathways, including mTOR signaling (P = 0.0301), glycosaminoglycan biosynthesis-chondroitin sulfate/dermatan sulfate (P = 0.0391), glycosaminoglycan biosynthesis-keratan sulfate (P = 0.0278), and PI3K-Akt signaling (P = 0.0243). CONCLUSION: This study identified different molecular features between Kashin-Beck disease and primary osteoarthritis and provided novel clues for clarifying the pathogenetic differences between KBD and OA. SN - 1478-6362 UR - https://www.unboundmedicine.com/medline/citation/29514696/Integrating_genome_wide_DNA_methylation_and_mRNA_expression_profiles_identified_different_molecular_features_between_Kashin_Beck_disease_and_primary_osteoarthritis_ L2 - https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-018-1531-1 DB - PRIME DP - Unbound Medicine ER -