Overexpression of progrmmed cell death 5 factor enhances triptolides-induced fibroblast-like synoviocytes apoptosis in rheumatoid arthritis
- VernacularTitle:程序化细胞死亡因子5过表达促进雷公藤内醇酯诱导的类风湿关节炎成纤维样滑膜细胞凋亡
- Author:
Zhankun CHEN
;
Ning WANG
;
Houshan LV
- Publication Type:Journal Article
- Keywords:
PDCD5;
Arthritis,rheumatoid;
Synovial membrane;
Apoptosis
- From:
Journal of Peking University(Health Sciences)
2003;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effect of progrmmed cell death 5(PDCD5)on apoptosis of rheumatoid arthritis fibroblast-like synoviocytes(RA FLS) induced by triptolide.Methods:Cultured synovial cells in vitro from RA patients were transfected with Ad-PDCD5.At protein level,expression of PDCD5 in RA FLS infected with Ad-PDCD5 was detected by Western blot.RA FLS infected with Ad-PDCD5 were cultured in presence or absence of triptolide and apoptosis of RA FLS was determined by flow cytometry.Results:Infection of RA FLS with increasing concentrations of Ad-PDCD5(50-300 MOI) resulted in a does-dependent increase in the production of PDCD5.Apoptotic cells percentage for noinfection group,Ad-null group and Ad-PDCD5 group were(22.41?3.87)%,(28.77?12.97)% and(48.87?12.69)%,respectively.Alternatively,infection without addition of triptolide stimuli had no effect.The data showed that gene transfection of PDCD5 alone without addition of triptolide was not sufficient to activate RA FLS apoptosis,PDCD5 acted as an enhancer rather than inductor of apoptosis.Conclusion:Overexpression of PDCD5 could enhance apoptosis of RA FLS induced by triptolide,PDCD5 may be a potential therapeutic target to RA.
