作者: T. Aizawa , T. Kon , T. A. Einhorn , L. C. Gerstenfeld
DOI: 10.1016/S0736-0266(00)00078-4
关键词: Fas receptor 、 Apoptosis 、 Molecular biology 、 Cell killing 、 Cartilage 、 Tumor necrosis factor alpha 、 Chondrocyte 、 Biology 、 Endochondral ossification 、 DNA fragmentation
摘要: Tumor necrosis factor alpha (TNF-alpha) induces apoptosis in a number of cell types and plays an essential role bone remodeling, both stimulating the proliferation osteoblasts activating osteoclasts. During endochondral ossification, chondrocytes occurs concurrently with new formation resorption replacement mineralized cartilage woven bone. In present study, TNF-alpha promoting chondrocyte was examined. Chondrocyte populations, enriched either hypertrophic or non-hypertrophic cells, were isolated from cephalic caudal portions 17-day chick embryo sterna, respectively, treated vitro 0.1-10 nM recombinant human TNF-alpha. As positive control, also induced by Fas receptor antibody binding. Dye exclusion assays live/dead ratios cells showed that caused dose-dependent 1.5- 2.0-fold increase dead chondrocytes. Induction independently assayed measurement interleukin-1beta-converting enzyme (ICE) activity, analyzed semi-quantitative determination DNA fragmentation. When compared to untreated these analyses increases levels ICE activity for all doses (from approximately 5 20 fold). Osteoblasts, however, not affected treatment antibody/protein G induction. Immunostaining caspase-2 protein expression most expressed two markers after Although killing induction higher more populations. These results demonstrate may be through mediated signaling, suggest are sensitive apoptotic effects within skeletal lineage than osteoblasts.