A preliminary study on the pathogenesis of neutrophil extracellular traps in rheumatoid arthritis
10.3760/cma.j.issn.1007-7480.2019.05.004
- VernacularTitle:中性粒细胞胞外诱捕网在类风湿关节炎致病机制中的初步探究
- Author:
Hui ZHANG
1
,
2
;
Yuchen FENG
;
Guorong KANG
;
Jinwu LIU
;
Sigong ZHANG
;
Haili SHEN
Author Information
1. 兰州大学第二临床医学院风湿免疫科 730030
2. 甘肃省疾病预防控制中心病原生物实验室
- Keywords:
Neutrophil extracellular traps;
Arthritis,rheumatoid;
Rheumatoid arthritis fibroblast-like synoviocytes;
Connective tissue growth factor
- From:
Chinese Journal of Rheumatology
2019;23(5):305-308,后插1
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the potential effects of neutrophil extracellular traps (NETs) on rheumatoid arthritis synovial fibroblasts (RA-FLSs).Methods The synovial tissues of RA patients were isolated and cultured in vitro.Peripheral blood neutrophils were extracted from healthy volunteers and used to stimulate NETs' formation,following with NETs' extraction.MTS proliferation assay was used to evaluate the effect of NETs on the proliferation of RA-FLSs.QRT-polymerase chain reaction (q-PCR) was used to determine the expression of connective tissue growth factor (CTGF) mRNA in cells treated with NETs-stimulated RA-FLSs for 60 h.The results were processed using paired sample t-test and one-way analysis of variance (ANOVA).Results The isolated and purified neutrophils could form NETs by in vitro stimulation.The concentration of extracted NETs-DNA was 58.5 ng/μl (1×106 cells).Compared with the control group (0 μl NETs),NETs could promote the proliferation of RA-FLSs.With the increase of NETs' concentration,the proliferation of RA-FLSs was also enhanced (F=99.519,P＜0.05).Compared with the control group (0 μl NETs),10 μl NETs could significandy promote the proliferation of RA-FLSs (t=-12.226,P＜0.01).Pretreatment of NETs with DNase Ⅰ inhibited its effect on promoting the proliferation of RA-FLSs (t=-2.376,P=0.049),NETs stimulated the upre-gulation of CTGF mRNA expression in RA-FLSs [(30.7±0.5),t=12.13,P＜0.01].Conclusion NETs can promote the proliferation of RA-FLSs and stimulate the up-regulation of CTGF mRNA in RA-FLSs in vitro.
