Δευτέρα 25 Απριλίου 2016

AMD3100 Attenuates Matrix Metalloprotease-3 and -9 Expressions and Prevents Cartilage Degradation in a Monosodium Iodo-Acetate–Induced Rat Model of Temporomandibular Osteoarthritis

Publication date: May 2016
Source:Journal of Oral and Maxillofacial Surgery, Volume 74, Issue 5
Author(s): Xiao-yan Wang, Yan Chen, Xue-jiao Tang, Lin-hong Jiang, Ping Ji
PurposeTemporomandibular joint osteoarthritis (TMJOA) is an important subtype of temporomandibular disorder. This study investigated the inflammatory role of the stromal cell-derived factor-1 (SDF-1) and C-X-C chemokine receptor-4 (CXCR4) axis and the probable signaling pathway involved in matrix metalloprotease (MMP)-3 and MMP-9 productions stimulated by the SDF-1–CXCR4 axis in an experimental rat model of TMJOA.Materials and MethodsRats were randomly divided into a control group, a pathologic model group, and an AMD3100 group. Effects of the bicyclam derivative AMD3100 (the specific antagonist of SDF-1–CXCR4 axis) were studied in TMJOA experimentally induced by monosodium iodo-acetate. Productions of SDF-1 and CXCR4 were compared in the normal and pathologic model groups, and cartilage changes and expressions of MMP-3, MMP-9, and phosphorylated extracellular signal-regulated kinase (p-ERK) were compared in the control, pathologic model, and AMD3100 groups.ResultsExpressions of SDF-1 and CXCR4 in the pathologic model group were increased compared with the control group (P < .05). Releases of MMP-3, MMP-9, and p-ERK and cartilage changes were downregulated in the AMD3100 group compared with the pathologic model group (P < .05), and these changes occurred in a dose-dependent manner with AMD3100 concentrations. Moreover, there were strong predictive relations between the expression of p-ERK with MMP-3 (r2 = 0.419; P < .001) and with MMP-9 (r2 = 0.542; P < .001).ConclusionsThe SDF-1–CXCR4 signaling pathway plays a proinflammatory role in experimental TMJOA, the bicyclam derivative AMD3100 can alleviate the severity of experimental TMJOA, and there might be a potential relation between the SDF-1–CXCR4 axis and the ERK signaling pathway.



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