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Nerve growth factor and ceramides modulate cell death in the early developing inner ear
L M Frago1, Y León, E J de la Rosa
1Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Cientificas, Madrid, Spain.
Journal of Cell Science
|May 30, 1998
Summary
Nerve growth factor and ceramide signaling regulate cell death in developing otic vesicles. Insulin-like growth factor-I counteracts ceramide-induced apoptosis, highlighting sphingomyelin pathway
Area of Science:
- Developmental Biology
- Cell Signaling
- Neuroscience
Background:
- Normal development relies on balancing cell division, differentiation, and death.
- The sphingomyelin pathway, initiated by ceramide, is known to signal apoptosis via nerve growth factor (NGF) and p75 receptors.
Purpose of the Study:
- To investigate signaling mechanisms regulating the balance between cell proliferation and apoptosis in the otic vesicle.
- To elucidate the role of the sphingomyelin pathway in otic vesicle development.
Main Methods:
- Organotypic cultures of otic vesicles were used.
- Stimulation with nerve growth factor (NGF) and ceramide.
- Assessment of apoptotic responses and the effects of insulin-like growth factor-I (IGF-I) and ceramide-1-phosphate.
Main Results:
- NGF stimulates sphingomyelin hydrolysis and ceramide release in otic vesicle cultures.
- Both NGF and ceramide induce apoptosis, with varying degrees.
- IGF-I suppressed ceramide-induced apoptosis.
- Ceramide-1-phosphate protected against serum withdrawal-induced apoptosis but not ceramide-induced cell death.
Conclusions:
- Sphingomyelin-derived second messengers, particularly ceramide, play a significant role in modulating programmed cell death during otic vesicle development.
- The balance between pro-apoptotic (ceramide) and pro-survival (IGF-I) signals is crucial for normal inner ear development.