Background: IGF1 protects mammalian hair cells in animal models from various types of damage, including aminoglycoside. Moreover, clinical trials have revealed that IGF1 was effective for idiopathic sudden sensorineural hearing loss. In this process, activation of the downstream of IGF1 signaling, including the phosphorylation of extracellular signal-regulated kinase (ERK) and AKT proteins, is involved. However, the regulation of IGF1 signaling mediators at the transcriptional level has not been studied.
Methods: We used a neomycin damage model on neonatal mouse cochlear explant culture. Explants established from neonatal mice were treated with either neomycin alone or neomycin and IGF1. The expression levels of IGF1 signaling mediator genes, Akt1, Mapk3, and Mapk1, in the explants were compared using quantitative reverse transcriptase-polymerase chain reaction at several time points. Inhibitors of IGF1 signaling were added to confirm that this observation was dependent on IGF1 signaling.
Results: The expression levels of all genes tested were significantly upregulated in neomycin+IGF1 treatment samples (p