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Fig. 4 | Arthritis Research & Therapy

Fig. 4

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

Fig. 4

Small interfering Toll-like receptor 2 (siTLR-2) knockdown of endogenous TLR-2 expression inhibits 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f)-mediated catabolic pathways in human chondrocytes. a To investigate the effect of TLR-2 on 29-kDa FN-f-induced signal pathways, human chondrocytes were transfected using control small interfering RNA (siRNA) or siTLR-2. After transfection, the cells were stimulated using 29-kDa FN-f for the indicated times, and the levels of phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (p-IκBα), phosphorylated c-Jun N-terminal kinase (p-JNK), phosphorylated p38 (p-p38), and phosphorylated extracellular signal-regulated kinase (p-ERK) were determined using Western blot analysis. Western blot data are representative of three independent experiments from different donors with similar results. b The relative phosphorylation level of JNK, ERK, p38, and IκBα proteins. Protein density was normalized to the respective unphosphorylated proteins. The bars represent the mean ± SD of three independent experiments from different donors with similar results. *P < 0.05 and **P < 0.01 vs. control siRNA-transfected chondrocytes. Ctl, control

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