Interleukin-17 regulates the proliferation of fibroblast-like synoviocytes of rheumatoid arthritis through signal transducer and activator of transcription 3 signaling
10.3760/cma.j.issn.1007-7480.2016.10.010
- VernacularTitle:白细胞介素-17通过信号转导与转录激活因子3调节类风湿关节炎成纤维样滑膜细胞的增殖
- Author:
Xiuyan SUN
;
Wei GAO
- Publication Type:Journal Article
- Keywords:
Arthritis rheumatoid;
Fibroblast-like synoviocytes;
Interleukin-17;
Signal transducer and activator of transcription 3
- From:
Chinese Journal of Rheumatology
2016;20(10):698-701
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine the effect of interleukin (IL)-17 on the proliferation of fibroblastlike synoviocytes (FLSs) from rheumatoid arthritis (RA)patients and to investigate whether signal transducer and activator of transcription 3 (STAT3) was implicated in this process.Methods FLSs were acquired by primary culturing from RA patients.STAT3,p-STAT3,Bcl-2 and Bax expression in FLSs were determined using western blotting analysis.The proliferation of FLSs was determined by MTT assay.Analysis of variance was used to determine the differences between two groups.Results IL-17 promoted the proliferation of FLSs from RA patients and inhibited their apoptosis.The pro-apoptotic Bax was decreased and anti-apoptotic Bcl-2 was increased in FLSs from RA (t=2.612,P＜0.05;t=2.723,P＜0.05).However,targeted silencing of STAT3 could inhibit the effect of IL-17 on FLSs (t=2.745,P＜0.05).[the control group:Bax (3.814±1.623),Bcl-2 (1.429± 0.311);IL-17 group:Bax (0.972±0.017),Bcl-2 (3.175±1.356);STAT3 silent group:Bax (5.729±1.236),Bcl-2 (0.637±0.006)].Conclusion STAT3 is critical in IL-17-induced proliferation of FLS from RA patients.IL-17/STAT3 pathway might be a good candidate for RA treatment modalities.
