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P120‐Catenin Mediates Intermittent Cyclic Mechanical Tension‐Induced Inflammation in Chondrocytes
Author(s) -
Xu Hongguang,
Gao Zhi,
Ma Mingming,
Xu Jiajia,
Xiao Liang,
Wang Hong,
Zhang Tao,
Liu Xiang,
Xu Yongming,
Zhang Xiaoling
Publication year - 2017
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26108
Subject(s) - chondrocyte , inflammation , chemistry , western blot , microbiology and biotechnology , catenin , nf κb , immunofluorescence , cartilage , signal transduction , wnt signaling pathway , in vitro , biology , immunology , anatomy , biochemistry , antibody , gene
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. 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. 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. P120‐catenin prevents endplate chondrocytes from undergoing ICMT‐mediated inflammation by suppressing the expression of NF‐κB. J. Cell. Biochem. 118: 4508–4516, 2017. © 2017 Wiley Periodicals, Inc.