Insulin-like growth factor 1 induces the transcription of Gap43 and Ntn1 during hair cell protection in the neonatal murine cochlea

- We found that Gap43 and Ntn1 were up-regulated by IGF-1 in the process of hair cell protection.
- The expression of Gap43 and Ntn1 was dependent on both the PI3K/Akt and MEK/ERK pathways.
- The up-regulation of Gap43 and Ntn1 transcripts were transient.

We previously reported that insulin-like growth factor 1 (IGF-1) protects cochlear hair cells against aminoglycosides through activation of the PI3K/Akt and MEK/ERK pathways in supporting cells. In this study, we found that IGF-1 up-regulated the expression levels of Gap43 and Ntn1 as measured using cDNA microarray analysis and qRT-PCR. Using inhibitors of the PI3K/Akt and MEK/ERK pathways, we reveal that both pathways are involved in the up-regulation of Gap43 and Ntn1 expression. Moreover the time window of Gap43 and Ntn1 transcription was limited to within 12 h after IGF-1 treatment, indicating that downstream gene expression was tightly controlled by IGF-1.