The plasmic translocation and release of high mobility group box chromosomal protein 1 in peripheral blood monocytes of patients with rheumatoid arthritis and the effect of thalidomide
- VernacularTitle:高迁移率族蛋白-1在类风湿关节炎患者单核细胞中的移位和释放及沙立度胺对其的影响
- Author:
Xiaoxia ZUO
;
Yanhui GONG
;
Yaou ZHOU
;
Hui LUO
;
Xianzhong XIAO
- Publication Type:Journal Article
- Keywords:
Arthritis,rheumatoid;
Monocytes;
Hiish mobility group box chromosomal protein 1;
Thalidomide
- From:
Chinese Journal of Internal Medicine
2008;47(5):374-377
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the release and intracellular localization of high mobility group box chromosomal protein 1(HMGBl)in the peripheral blood monocytes of rheumatoid arthritis(RA) patients and the inhibitive effect of thaiidomide.Methods 19 RA patients and 20 healthy controls were included in the study.Monocytes were separated from peripheral blood with Ficoll density gradient centrifugation.Monocytes were treated with 100 ng/ml tumor necrosis factor α(TNFa)or 100 ng/ml TNFα plus 40 μg/ml thalidomide and grown in an incubator at 37℃ with 5%CO,for 24 hours.The cuIture supernatants of the monocytes were collected.HMGB1 level in the culture medium was detected with Western blot.In addition,the intraceUular localization of HMGB1 in the fflonocytes was investigated with immunocytochemical analysis. Results Without stimulation. the release of HMGBl protein was significantly increased in the culture supernatants of peripheral blood monocytes from RA patients as compared with that from healthy controls(P<0.05).TNFα(100 ng/ml)did not further increase the release of HMGBl in the monocytes from the patients with RA.Thalidomide(40 μg/ml)could inhibit the release of HMGB1 in the monocytes from RA patients stimulated with TNFα(P<0.05).In the monocytes from RA patients,HMGBl was mainly localized in the nucleus.Treatment with TNFOL(100 ng/ml)for 24 hour resulted in a cytoplasmic translocation of HMGB1,which was inhibited significantly by thalidomide. Conclusion TNFα induces the release and cytoplasmic translocation of HMGBI in the peTipheral blood monocytes of RA patients and thalidomide inhibits the release and translocation of HMGB1.
