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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: METHODS, OBJECTIVE, BACKGROUND, METHODS, RESULTS. Meshes: Animals, Antibodies, Monoclonal, Antibody Affinity, Apoptosis, Cells, Cultured, Chondrocytes, Fas Ligand Protein, Insulin-Like Growth Factor I, Integrin alpha1, Membrane Glycoproteins, Rats, Rats, Sprague-Dawley, Tumor Necrosis Factors, fas Receptor.
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Does insulin-like growth factor-1 treatment prevent anti-Fas antibody-induced apoptosis in endplate chondrocytes? Context: 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.
assistant
Fas antibody induces apoptosis and decreases Integrin-alpha1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes. Final Decision: yes