Tumor necrosis factor-α up-regulates the expression of β1,4-Galactosyltransferase-Ⅰ in fibroblast-like synoviocytes of osteoarthritis
10.3760/cma.j.issn.1007-7480.2013.10.008
- VernacularTitle:肿瘤坏死因子-α在骨关节炎成纤维样滑膜细胞中上调β1,4-乳糖基转酶-Ⅰ的表达
- Author:
Xinhui ZHU
;
Dawei XU
;
Wei LIU
;
Shengyu CUI
;
Wei HUANG
;
Zhiming CUI
- Publication Type:Journal Article
- Keywords:
Tumor necrosis factor-alpha;
Lipopolysaccharides;
Osteoarthritis;
Fibroblast-like synoviocytes;
β1,4-galactosyltransferase-Ⅰ
- From:
Chinese Journal of Rheumatology
2013;17(10):681-684,后插2
- CountryChina
- Language:Chinese
-
Abstract:
Objective To analyze whether β1,4-galactosyltransferase-Ⅰ(β1,4-GaiT-Ⅰ)expression correlates with the expression of tumor necrosis factor(TNF)-α in osteoarthritis(OA).Methods Synovial tissue samples from eight OA patients and eight healthy people were obtained as the experimental group and controls respectively.The mRNA levels of β1,4-GalT-Ⅰ and TNF-α were measured by reverse transcriptionpolymerase chain reaction(RT-PCR)and real-time PCR.Enzyme linked immunosorbent assay(ELISA)was used to test the expression of TNF-α in the protein level.Cellular colocalization of β1,4-GalT-Ⅰ and TNF-α was analyzed by double immunofluorescence.ANOVA and t-test was used for statistical analysis.Results ①Compared with the control group[β1,4-GalT-Ⅰ(0.48±0.09),TNF-α(0.46±0.07)],the expression of β1,4-GalT-Ⅰ(0.94±0.16)and TNF-α(1.19±0.19)were significantly increased in OA synovial tissue(t=3.47,t=4.06,P＜0.01)and there was colocalization between β1,4-GalT-Ⅰ and TNF-α;② Lipopolysaccharide (LPS)could induce fibroblast-like synoviocytes(FLSs)β1,4-GalT-Ⅰ[11.2±0.9 vs 2.9±0.5(dose effect),22.3±2.3 vs 4.4±0.9(time effect),F=83.03,F=157.58,P＜0.05]overexpression;③ LPS could induce FLSs TNF-α[(1256±96)vs(101±7)pg/ml,F=431.96,P＜0.01]overexpression;④ Not only endogenous TNF-α,but exogenous TNF-α could induce FLSs β1,4-GalT-Ⅰ[23.2±1.9 vs 8.4±1.3(dose effect),23.9±1.8 vs 11.5±1.3(time effect),F=124,F=93.6,P＜0.05]overexpression.Conclusion It is possible that FLSs mayuse TNF-αto control β1,4-GalT-Ⅰ functions during inflammation in OA.
