• Yong-Jun Wang, Qi Shi, Peng Sun, Quan Zhou, Michael Darowish, Tian-Fang Li, Yu-Feng Dong, William W Lu, and John C Y Leong.
• Institute of Spine, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Yongjun_wang@urmc.rochester.edu
• Spine. 2006 Apr 1; 31 (7): 736-41.

Study DesignIn vitro investigation of vertebral endplate chondrocyte apoptosis.ObjectivesTo determine whether Fas antibody caused apoptosis in endplate chondrocytes, and whether insulin-like growth factor-1 (IGF-1) inhibited this effect. Integrin-alpha1 and focal adhesion kinase (FAK) expression in conjunction with apoptosis was also investigated.Summary Of Background DataBinding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects.Materials And MethodsRat cervical endplate chondrocytes were cultured and treated with Fas antibody, with or without IGF-1. Cellular morphology was examined by microscopy. Apoptotic changes were evaluated by transmission electron microscopy, TUNEL staining, and immunostaining. Apoptosis-induced changes in the expression of integrin-alpha1 chain and FAK were also investigated.ResultsEndplate chondrocytes were able to be cultured; a chondrocytic phenotype was maintained. Fas antibody induced apoptosis in endplate chondrocytes; this was confirmed by TUNEL staining. Bcl-2 expression was decreased by Fas antibody, while Bax expression increased. Integrin-alpha1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes.ConclusionsFas antibody induces apoptosis and decreases Integrin-alpha1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes.

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