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

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài:The expression of the receptor for advanced glycation end-products (RAGE) in RA-FLS is induced by IL-17 via Act-1. | Heo et al. Arthritis Research Therapy 2011 13 R113 http content 13 4 R113 RESEARCH ARTICLE Open Access The expression of the receptor for advanced glycation end-products RAGE in RA-FLS is induced by IL-17 via Act-1 11 1 t 2 t 14 t 1 1 1 Yu-Jung Heo Hye-Jwa Oh Young Ok Jung Mi-La Cho Seon-Yeong Lee Jun-Geol Yu Mi-Kyung Park Hae-Rim Kim3 Sang-Heon Lee3 Sung-Hwan Park1 2 and Ho-Youn Kim1 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-KB NF-kB 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-13 P vs. untreated cells treatment but not by tumor necrosis factor TNF -a in RA-FLS. The combined stimuli of both IL-17 and IL-13 significantly increased RAGE production compared to a single stimulus with IL-17 or IL-13 alone P 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-13. Act-1 contributed to the stimulatory effect of IL-17 on RAGE production suggesting a possible inhibitory target for RA treatment. Introduction Rheumatoid arthritis RA is a systemic autoimmune disease characterized by .

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