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Transforming growth factor ß1 inhibition protects from noise-induced hearing loss

AutorMurillo-Cuesta, Silvia ; Rodriguez-de la Rosa, Lourdes ; Contreras, Julio ; Celaya, Adelaida M. ; Camarero, Guadalupe ; Rivera, Teresa ; Varela-Nieto, Isabel
Palabras claveProtection
Cochlear injury
Inflammation
Noise-induced hearing loss
TGF-β
Fecha de publicación2015
EditorFrontiers Media
CitaciónFrontiers in Aging Neuroscience 7: 32 (2015)
ResumenExcessive exposure to noise damages the principal cochlear structures leading to hearing impairment. Inflammatory and immune responses are central mechanisms in cochlear defensive response to noise but, if unregulated, they contribute to inner ear damage and hearing loss. Transforming growth factor ß (TGF-ß) is a key regulator of both responses and high levels of this factor have been associated with cochlear injury in hearing loss animal models. To evaluate the potential of targeting TGF-ß as a therapeutic strategy for preventing or ameliorating noise-induced hearing loss, we studied the auditory function, cochlear morphology, gene expression and oxidative stress markers in mice exposed to noise and treated with TGF-ß1 peptidic inhibitors P17 and P144, just before or immediately after noise insult. Our results indicate that systemic administration of both peptides significantly improved both the evolution of hearing thresholds and the degenerative changes induced by noise-exposure in lateral wall structures. Moreover, treatments ameliorated the inflammatory state and redox balance. These therapeutic effects were dose-dependent and more effective if the TGF-ß1 inhibitors were administered prior to inducing the injury. In conclusion, inhibition of TGF-ß1 actions with antagonistic peptides represents a new, promising therapeutic strategy for the prevention and repair of noise-induced cochlear damage.
DescripciónThis is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).
Versión del editorhttp://dx.doi.org/10.3389/fnagi.2015.00032
URIhttp://hdl.handle.net/10261/124616
DOI10.3389/fnagi.2015.00032
Identificadoresdoi: 10.3389/fnagi.2015.00032
issn: 1663-4365
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