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Fig. 3 | Arthritis Research & Therapy

Fig. 3

From: Fibronectin fragment-induced expression of matrix metalloproteinases is mediated by MyD88-dependent TLR-2 signaling pathway in human chondrocytes

Fig. 3

Increased Toll-like receptor (TLR)-2 expression promotes 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f)-induced matrix metalloproteinase (MMP) production in normal and osteoarthritis (OA) chondrocytes. Human chondrocytes were transfected using a TLR-2 expression vector or empty vector as a control. a TLR-2 expression was upregulated in chondrocytes transfected with TLR-2 expression vectors. b TLR-2 overexpression significantly increased MMP-1, MMP-3, and MMP-13 mRNA expression compared with cells transfected with empty vector. The mRNA expression level in untreated control small interfering RNA transfected chondrocytes was set as 1. Data represent the mean ± SD for triplicate experiments from three different donors. *P < 0.05, **P < 0.01, and ***P < 0.001 vs. control. c The 29-kDa FN-f-induced release of MMP-1 and MMP-3 was analyzed using Western blot analysis. TLR-2 overexpression enhanced the synthesis of MMP-1 and MMP-3 in normal and OA chondrocytes. d MMP-13 production in culture supernatants was determined by enzyme-linked immunosorbent assay. The 29-kDa FN-f-induced MMP-13 production was significantly higher in cells transfected with the TLR-2 expression vector. The bars represent the mean ± SD of triplicate samples from three different donors. *P < 0.05 and **P < 0.01 vs. empty vector-transfected chondrocytes

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