Insulin-Like Growth Factor-1 Treatment Prevents Anti-Fas Antibody-Induced Apoptosis in Endplate Chondrocytes

Autor: Michael Darowish, Peng Sun, William W. Lu, Qi Shi, Tian Fang Li, Quan Zhou, Yong-Jun Wang, John C. Y. Leong, Yufeng Dong
Rok vydání: 2006
Předmět:
Zdroj: Spine. 31:736-741
ISSN: 0362-2436
DOI: 10.1097/01.brs.0000208128.49912.64
Popis: 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.
Databáze: OpenAIRE