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Identification of differentially expressed genes and pathways between primary osteoarthritis and endemic osteoarthritis (Kashin–Beck disease)
Key Laboratory of Environment and Gene Related Diseases, Ministry of Education, Faculty of Public Health, College of Medicine, Xi’an Jiaotong University, Xi’an, Shaanxi, China.
Key Laboratory of Environment and Gene Related Diseases, Ministry of Education, Faculty of Public Health, College of Medicine, Xi’an Jiaotong University, Xi’an, Shaanxi, China.
Key Laboratory of Environment and Gene Related Diseases, Ministry of Education, Faculty of Public Health, College of Medicine, Xi’an Jiaotong University, Xi’an, Shaanxi, China.
Key Laboratory of Environment and Gene Related Diseases, Ministry of Education, Faculty of Public Health, College of Medicine, Xi’an Jiaotong University, Xi’an, Shaanxi, China.
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2013 (English)In: Scandinavian Journal of Rheumatology, ISSN 0300-9742, E-ISSN 1502-7732, Vol. 42, no 1, 71-79 p., 23157206Article in journal (Refereed) Published
Abstract [en]

Objectives: Primary osteoarthritis (OA) and Kashin–Beck disease (KBD) exhibit similar clinical manifestations and common articular cartilage lesions. Revealing the pathogenetic differences between OA and KBD is helpful for differential diagnosis and may provide new insights into the pathogenesis of OA and KBD. In this study, we compared the genome-wide gene ontology (GO) and pathway expression patterns of articular cartilage derived from both OA and KBD patients.

Methods: Total RNA was isolated, amplified, labelled, and hybridized using Agilent whole genome microarray analysis. Gene set enrichment analysis (GSEA) was used to identify differentially expressed genes and pathways between OA and KBD. Nine differentially expressed GO categories and 85 differentially expressed pathways were identified by this study.

Results: The reactive oxygen species (ROS)-related HOUSTIS_ROS pathway and the vascular endothelial growth factor (VEGF)-related ABE_VEGFA_TARGETS_2HR pathway were significantly up-regulated in OA compared to KBD. Higher expression levels of the collagen-related COLLAGEN GO, EXTRACELLULAR_MATRIX_PART GO, and nitric oxide (NO)-related BIOCARTA_NO1_PATHWAY pathways were detected in KBD than in OA.

Conclusions: ROS-induced cartilage lesions seem to be more involved in the pathogenesis of OA whereas NO-mediated chondrocyte apoptosis contributes more to the development of KBD.

Place, publisher, year, edition, pages
Informa Healthcare, 2013. Vol. 42, no 1, 71-79 p., 23157206
Keyword [en]
Kashin-Beck disease, Osteoarthritis, Expression profiling, Pathway analysis, Gene set enrichment analysis
National Category
Cell and Molecular Biology Orthopedics
Research subject
Genetics; Medicine, rheumatology; Orthopaedics
Identifiers
URN: urn:nbn:se:umu:diva-104358DOI: 10.3109/03009742.2012.698303OAI: oai:DiVA.org:umu-104358DiVA: diva2:819277
Available from: 2015-06-10 Created: 2015-06-10 Last updated: 2015-06-10

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Lammi, Mikko
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