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Título: | Programmed cell death in the developing inner ear is balanced by nerve growth factor and insulin-like growth factor I |
Autor: | Frago, Laura M.; Cañón, Susana CSIC; De la Rosa, Enrique J. CSIC ORCID ; León, Yolanda CSIC ORCID; Varela-Nieto, Isabel CSIC ORCID | Palabras clave: | P75 neurotrophin receptor (p75NTR) Ceramide Caspase activation Cell survival Otic vesicle Ceramide-1-phosphate |
Fecha de publicación: | 1-feb-2003 | Editor: | Company of Biologists | Citación: | Journal of Cell Science 116(3): 475-486 (2003) | Resumen: | Nerve growth factor induces cell death in organotypic cultures of otic vesicle explants. This cell death has a restricted pattern that reproduces the in vivo pattern of apoptosis occurring during inner ear development. In this study, we show that binding of nerve growth factor to its low affinity p75 neurotrophin receptor is essential to achieve the apoptotic response. Blockage of binding to p75 receptor neutralized nerve-growth-factor-induced cell death, as measured by immunoassays detecting the presence of cytosolic oligonucleosomes and by TUNEL assay to visualize DNA fragmentation. Nerve growth factor also induced a number of cell-death-related intracellular events including ceramide generation, caspase activation and poly-(ADP ribose) polymerase cleavage. Again, p75 receptor blockade completely abolished all of these effects. Concerning the intracellular pathway, ceramide increase depended on initiator caspases, whereas its actions depended on both initiator and effector caspases, as shown by using site-specific caspase inhibitors. Conversely, insulin-like growth factor I, which promotes cell growth and survival in the inner ear, abolished apoptosis induced by nerve growth factor. Insulin-like growth factor cytoprotective actions were accomplished, at least in part, by decreasing endogenous ceramide levels and activating Akt. Taken together, these results strongly suggest that regulation of nerve-growth-factor-induced apoptosis in the otocysts occurs via p75 receptor binding and is strictly controlled by the interaction with survival signalling pathways. | Descripción: | 12 pages, 6 figures, 4 tables. | Versión del editor: | http://dx.doi.org/10.1242/jcs.00223 | URI: | http://hdl.handle.net/10261/24671 | DOI: | 10.1242/jcs.00223 | ISSN: | 0021-9533 |
Aparece en las colecciones: | (IIBM) Artículos (CIB) Artículos |
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Programmed cell death.pdf | 928,42 kB | Adobe PDF | Visualizar/Abrir |
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