Gene Expression Profile in Patients with Axial Spondyloarthritis: Meta-analysis of Publicly Accessible Microarray Datasets.
10.4078/jrd.2016.23.6.363
- Author:
Robin PARK
1
;
Tae Hwan KIM
;
Jong Dae JI
Author Information
1. Division of Rheumatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea. jjdjmesy@korea.ac.kr
- Publication Type:Meta-Analysis ; Original Article
- Keywords:
Axial spondyloarthritis;
Ankylosing spondylitis;
Microarray;
Network analysis
- MeSH:
Dataset*;
Gene Expression*;
Genes, vif;
Hand;
Humans;
Interleukin-17;
Interleukin-7;
Osteoclasts;
Receptors, Antigen, T-Cell;
Spondylitis;
Spondylitis, Ankylosing;
Synovial Membrane;
Toll-Like Receptors;
Transcriptome*;
Transducers
- From:Journal of Rheumatic Diseases
2016;23(6):363-372
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: To identify a gene expression signature in axial spondyloarthritis/ankylosing spondylitis (SpA/AS) and genomic pathways likely to be involved in pathogenesis of SpA/AS patients. METHODS: Four publicly accessible microarray studies from SpA/AS patients were integrated, and a transcriptomic and network-based meta-analysis was performed. This meta-analysis was compared with a published microarray study in whole blood of AS patients. RESULTS: According to our meta-analysis, 1,798 genes were differentially expressed in the whole blood of SpA/AS patients compared to healthy controls, while 674 genes were differentially expressed in the synovium of SpA/AS patients compared to healthy controls. When the whole blood meta-analysis data was compared with a published microarray study that also analyzed whole blood in SpA/AS patients, pathways involved in Toll-like receptor signaling, osteoclast differentiation, T cell receptor signaling and janus kinase–signal transducer and activator of transcription (Jak-STAT) signaling were often enriched in SpA/AS. On the other hand, eomesodermin, RUNX3, and interleukin-7 receptor (IL7R) were usually decreased in SpA/AS patients, suggesting that deficiency of these genes contributes to increased IL-17 production in AS. CONCLUSION: Several common enrichment pathways including Toll-like receptor signaling pathway, osteoclast differentiation, T cell receptor signaling pathway and Jak-STAT signaling pathway were identified in the differentially expressed genes of whole blood and synovium from SpA/AS patients, suggesting that these pathways are involved in the pathogenesis of SpA/AS.
