Publication Date:
2017-05-03
Description:
Objective: To study the role of the nuclear factor (NF)-κB signaling pathway and P120-catenin in the inflammatory effects of intermittent cyclic mechanical tension (ICMT) on endplate chondrocytes. Design: Inflammatory reactions of endplate chondrocyte were measured by real-time reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assays, a dual-luciferase reporter assay system, immunofluorescence, and western blot analysis. Results: ICMT loading led to inflammatory reactions of endplate chondrocytes in both the rabbit endplate cartilage model and rat endplate chondrocytes in vitro. Inhibition of NF-κB signaling significantly ameliorated the inflammation induced by ICMT in endplate chondrocytes. Moreover, the expression of P120-catenin was decreased by ICMT. However, over-expression of P120-catenin suppressed NF-κB signaling and reversed the inflammatory effects. Conclusions: P120-catenin prevents endplate chondrocytes from undergoing ICMT-mediated inflammation by suppressing the expression of NF-κB. This article is protected by copyright. All rights reserved
Electronic ISSN:
0091-7419
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
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