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01.08.2011 | Research article | Ausgabe 4/2011 Open Access

Arthritis Research & Therapy 4/2011

The expression of the receptor for advanced glycation end-products (RAGE) in RA-FLS is induced by IL-17 via Act-1

Zeitschrift:
Arthritis Research & Therapy > Ausgabe 4/2011
Autoren:
Yu-Jung Heo, Hye-Jwa Oh, Young Ok Jung, Mi-La Cho, Seon-Yeong Lee, Jun-Geol Yu, Mi-Kyung Park, Hae-Rim Kim, Sang-Heon Lee, Sung-Hwan Park, Ho-Youn Kim
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​ar3398) contains supplementary material, which is available to authorized users.
Yu-Jung Heo, Hye-Jwa Oh, Young Ok Jung, Mi-La Cho contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

YJH, YOJ, and MLC contributed to conception and design, acquisition of data, analysis and interpretation of data, drafting of the article and final approval of the submitted manuscript. OHJ, JGY and SYL contributed to immunohistochemistry. HRK, MKP and SHL helped with PCR, Western blotting and ELISA, and SHP and HYK contributed cell culture and transfection. All authors approved the final manuscript.

Abstract

Introduction

The receptor for advanced glycation end-products (RAGE) has been implicated in the pathogenesis of arthritis. We conducted this study to determine the effect of interleukin (IL)-17 on the expression and production of RAGE in fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis (RA). The role of nuclear factor-κB (NF-κB) activator 1 (Act1) in IL-17-induced RAGE expression in RA-FLS was also evaluated.

Methods

RAGE expression in synovial tissues was assessed by immunohistochemical staining. RAGE mRNA production was determined by real-time polymerase chain reaction. Act-1 short hairpin RNA (shRNA) was produced and treated to evaluate the role of Act-1 on RAGE production.

Results

RAGE, IL-17, and Act-1 expression increased in RA synovium compared to osteoarthritis synovium. RAGE expression and production increased by IL-17 and IL-1β (*P <0.05 vs. untreated cells) treatment but not by tumor necrosis factor (TNF)-α in RA-FLS. The combined stimuli of both IL-17 and IL-1β significantly increased RAGE production compared to a single stimulus with IL-17 or IL-1β alone (P <0.05 vs. 10 ng/ml IL-17). Act-1 shRNA added to the RA-FLS culture supernatant completely suppressed the enhanced production of RAGE induced by IL-17.

Conclusions

RAGE was overexpressed in RA synovial tissues, and RAGE production was stimulated by IL-17 and IL-1β. Act-1 contributed to the stimulatory effect of IL-17 on RAGE production, suggesting a possible inhibitory target for RA treatment.
Zusatzmaterial
Authors’ original file for figure 1
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Literatur
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