From gene expression to serum proteins: biomarker discovery in ankylosing spondylitis

Objectives:Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).Methods:Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results...

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Vydané v:Annals of the rheumatic diseases Ročník 69; číslo 1; s. 297 - 300
Hlavní autori: Haroon, N, Tsui, F W L, O’Shea, F D, Chiu, B, Tsui, H W, Zhang, H, Marshall, K W, Inman, R D
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England BMJ Publishing Group Ltd and European League Against Rheumatism 01.01.2010
Elsevier Limited
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ISSN:0003-4967, 1468-2060, 1468-2060
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Shrnutí:Objectives:Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).Methods:Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results were confirmed by quantitative real-time (qRT)–PCR. Corresponding serum-soluble LIGHT (sLIGHT) was estimated by ELISA and the fold change in sLIGHT was correlated to the fold change in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and the Bath AS disease activity index.Results:Post-infliximab, 69% of the patients (11/16) achieved an ASAS20 response. Six candidate genes were differentially expressed by microarray; four of which were validated by qRT–PCR. sLIGHT showed the most significant difference. There was good correlation of baseline sLIGHT with CRP (R  =  0.60; p = 0.01) and ESR (R  =  0.51; p = 0.04). The fold change in sLIGHT correlated with change in both CRP (R  =  0.71, p = 0.002) and ESR (R  =  0.77, p<0.001).Conclusion:LIGHT is significantly downregulated by infliximab. sLIGHT correlated well with changes in inflammatory markers.
Bibliografia:href:annrheumdis-69-297.pdf
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ArticleID:ar102277
local:annrheumdis;69/01/297
PMID:19103635
ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0003-4967
1468-2060
1468-2060
DOI:10.1136/ard.2008.102277