P120-catenin Mediates Intermittent Cyclic Mechanical Tension Induced Inflammatory Effect In Chondrocyte

Objective: To study the role of NF-?B signaling pathway and P120-catenin in endplate chondrocytes inflammatory effect caused by ICMT.Methods: The chondrocytes of the lumbar vertebrae were obtained by trypsin digestion.The chondrocytes were cultured in the second-generation terminal chondrocytes.The platelet loading was induced by FX-5000 cell strain loading system.Cell inflammation model;the specific inhibitor Bay117082 regulates the NF-?B signaling pathway;transfectes the expression of the P120-catenin gene by gene transfection.Real-time RTPCR and Western blot were used to detect the expression of MMP3,MMP9,MMP13,COX-2,iNOS and other genes and proteins in the cartilage inflammatory medium.The AlamarBlue method was used to detect the rate of platelet chondrocytes.Flow cytometry And the expression of P120-catenin in the terminal chondrocytes was detected by immunofluorescence.The nuclear and cytoplasmic cytoplasmic NF-?B in the nucleus and cytoplasm were detected by immunofluorescence.NF-?B signaling pathway-related protein P65,p-P65,IkB?,p-IkB? expression changes;Dual-Luciferase reporter gene detection of NF-?B signaling pathway activation.Results: ICMT loading led to inflammatory reaction of endplate chondrocytes both in rabbit endplate cartilage model and rats endplate chondrocyte in vitro.Inhibition of NF-?B signaling pathway significantly ameliorated the inflammatory induced by ICMT in endplate chondrocyte.Meanwhile,the expression of P120-catenin was decreased by ICMT.However,over-expression of P120-catenin can restrain the NF-?B signaling pathway,and rescued the inflammatory.Conclusion: P120-catenin defend endplate chondrocytes from ICMT caused inflammation by suppressing the expression of NF-?B signaling pathway.