Insulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytes

Yong Jun Wang, Qi Shi, Peng Sun, Quan Zhou, Michael Darowish, Tian Fang Li, Yu Feng Dong, William W. Lu, John C.Y. Leong

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Study Design. In vitro investigation of vertebral endplate chondrocyte apoptosis. Objectives. To determine whether Fas antibody caused apoptosis in endplate chondrocytes, and whether insulin-like growth factor-1 (IGF-1) inhibited this effect. Integrin-ā1 and focal adhesion kinase (FAK) expression in conjunction with apoptosis was also investigated. Summary of Background Data. Binding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects. Materials and Methods. Rat 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-ā1 chain and FAK were also investigated. Results. Endplate 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-ā1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes. Conclusions. Fas antibody induces apoptosis and decreases Integrin-ā1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes.

Original languageEnglish (US)
Pages (from-to)736-741
Number of pages6
Issue number7
StatePublished - Apr 1 2006

All Science Journal Classification (ASJC) codes

  • Orthopedics and Sports Medicine
  • Clinical Neurology


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