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Varela-Nieto, I. et al.

Varela-Nieto, Morales-Garcia, Vigil, Diaz-Casares, Gorospe, Sánchez-Galiano, Cañon, Camarero, Contreras, Cediel, Leon,

Trophic effects of insulin-like growth factor-I (IGF-I) in the inner ear.

Insulin-like growth factors (IGFs) have a pivotal role during nervous system development and in its functional maintenance. IGF-I and its high affinity receptor ( IGF1R) are expressed in the developing inner ear and in the postnatal cochlear and vestibular ganglia. We recently showed that trophic support by IGF-I is essential for the early neurogenesis of the chick cochleovestibular ganglion (CVG). In the chicken embryo otic vesicle, IGF-I regulates developmental death dynamics by regulating the activity and/or levels of key intracellular molecules, including lipid and protein kinases such as ceramide kinase, Akt and Jun N-terminal kinase (JNK). Mice lacking IGF-I lose many auditory neurons and present increased auditory thresholds at early postnatal ages. Neuronal loss associated to IGF-I deficiency is caused by apoptosis of the auditory neurons, which presented abnormally increased levels of activated caspase-3. It is worth noting that in man, homozygous deletion of the IGF-1 gene causes sensory-neural deafness. IGF-I is thus necessary for normal development and maintenance of the inner ear. The trophic actions of IGF-I in the inner ear suggest that this factor may have therapeutic potential for the treatment of hearing loss.[1]

References

Trophic effects of insulin-like growth factor-I (IGF-I) in the inner ear. Varela-Nieto, I., Morales-Garcia, J.A., Vigil, P., Diaz-Casares, A., Gorospe, I., Sánchez-Galiano, S., Cañon, S., Camarero, G., Contreras, J., Cediel, R., Leon, Y. Hear. Res. (2004) [Pubmed]

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