Effects of interleukin-34 on prostaglandin E2 expression of fibroblast-like synoviocytes in patients with rheumatoid arthritis
10.3760/cma.j.issn.1007-7480.2017.01.008
- VernacularTitle:白细胞介素-34对类风湿关节炎成纤维样滑膜细胞前列腺素E2/环氧化酶2表达的影响
- Author:
Yawei TANG
;
Bing WANG
;
Xiaotong SUN
;
Zijian MA
;
Xia LI
;
Yan ZHANG
- Keywords:
Arthritis,rheumatoid;
Interleukins;
Dinoprostone;
Epoxy compounds;
Fibroblast-like synoviocytes
- From:Chinese Journal of Rheumatology
2017;21(1):37-41
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of interleukin-34 (IL-34) on prostaglandin E2 (PGE2)/cyclo-oxygenase-2 (COX-2) expression on fibroblast-like synoviocytes (FLS) in patients with rheumatoid arthritis (RA). Methods FLS was isolated from 6 RA patients and stimulated with IL-34 (50 ng/ml), IL-34 receptor antagonist (25 ng/ml) and IL-34 (50 ng/ml), inhibitors of signaling pathway (10 μmol/L) and IL-34 (50 ng/ml) in vitro respectively. The expression of COX-2 mRNA was detected by reverse transcription polymerase chain reac-tion (RT-PCR). The level of PGE2 in the supernatant of RA FLS culture was measured by Enzyme linked immunosorbent assay (ELISA). Statistical analysis between groups were performed by t test. Results Com-pared to unstimulated FLS, COX-2 and PGE2 expression was increased dramatically on IL-34-stimulated FLS, most evidently in 48 hours [(139±24) pg/ml vs (201±8) pg/ml, t=-6.177, P<0.01]; Moreover, the level of PGE2 was decreased when anti-IL-34 antibody was added to the IL-34-stimulated RA FLS at 24 hours, 48 hours, 72 hours [(250 ±58) pg/ml vs (100 ±28) pg/ml, t=5.742, P<0.01; (375 ±24) pg/ml vs (97 ±23) pg/ml, t=20.564, P<0.001; (357 ±21) pg/ml vs (94 ±18) pg/ml, t=22.353, P<0.01]; In the presence of SB203580 and IKK-16, PGE2 level produced by IL-34-stimulated FLS was obviously decreased [(279 ±37) pg/ml vs (63 ±17) pg/ml, t=12.806, P<0.01;(279±37) pg/ml vs (77±16) pg/ml, t=6.177, P<0.01]. Conclusion Binding of IL-34 with its receptor may promote the secretion of PGE2 via NF-κB and P38 MAPK signaling pathway in RA FLS, suggesting that it might be involved in the pathogenesis of RA.
