Mechanism of tumor necrosis factor-like weak inducer of apoptosis on the synthesis of Matrix meta-lloproteinase-1 in fibroblast-like synoviocytes of rheumatoid arthritis
10.3760/cma.j.issn.1007-7480.2009.09.012
- VernacularTitle:肿瘤坏死因子样凋亡的微弱诱导剂诱导成纤维样滑膜细胞合成基质金属蛋白酶-1机制的研究
- Author:
Liping XIA
;
Hui SHEN
;
Jing LU
;
Weiguo XIAO
- Publication Type:Journal Article
- Keywords:
Arthritis,rheumatoid;
Interstitial collagenase;
p38 mitogen-activated protein kinases
- From:
Chinese Journal of Rheumatology
2009;13(9):627-629
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study whether p38 mitogen-activated protein kinases (p38MAPK) signal pathway were activated in the process of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) which then induces rheumatoid arthritis (RA) fibroblast-like synoviocyte (FLS) to synthesize matrix metalloproteinase-1 (MMP-1) and look for the relative mechanisms of how TWEAK was involved in the destruction of articular bones and cartilage. Methods RA FLS were primarily cultured and stimulated with TWEAK. FLS were pretreated with SB203580 or not. ELISA was used to detect the concentration of MMP-1 in cell-cultured supernatant. Western blotting was used to detect the expression of p-p38MAPK and P65 in RA FLS. Results TWEAK (100 ng/ml) could induce RA FIS to synthesize MMP-1. SB203580 could partially inhibite the expression of MMP-1 producted by RA FLS which was induced by TWEAK. TWEAK could make p38MAPK phosphorylated and increase the expression of P65 protein in the cell nucleus. Conclusion TWEAK induces RA FLS to synthesize MMP-1. In this process, p38MAPK signal transduction pathway is activated and then induce the expression of NF-κB.
