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

Abstract

In vitro investigation of vertebral endplate chondrocyte apoptosis. To 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. Binding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects. 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-alpha1 chain and FAK were also investigated. 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-alpha1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes. Fas antibody induces apoptosis and decreases Integrin-alpha1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes.