Heat shock factor 1-deficient mice exhibit decreased recovery of hearing following noise overstimulation
✍ Scribed by Damon A. Fairfield; Margaret I. Lomax; Gary A. Dootz; Shu Chen; Andrzej T. Galecki; Ivor J. Benjamin; David F. Dolan; Richard A. Altschuler
- Book ID
- 102384236
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 308 KB
- Volume
- 81
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
✦ Synopsis
Heat shock proteins (Hsps) can enhance cell survival in response to stress. Heat shock factor 1 (Hsf1) is the major transcription factor that regulates stress-inducible Hsp expression. We previously demonstrated the presence of Hsf1 in the rodent cochlea and also demonstrated that a heat shock known to precondition the cochlea against noise trauma results in Hsf1 activation in the rodent cochlea. In the present study, we used an Hsf1-deficient (Hsf1-/- mouse model to determine whether eliminating the Hsf1-dependent stress pathway would influence hearing loss and/or recovery from a moderate-intensity noise. Hsf1-/- mice and their normal littermates (Hsf1+/+) were exposed to a 98-dB, broadband (2-20 kHz) noise for 2 hr, and auditory brainstem response thresholds were measured at three frequencies (4, 12, and 20 kHz) 3 hr, 3 days, and 2 weeks after noise. Hsf1-/- mice had greater hearing loss than Hsf1+/+ mice, with significant differences in recovery observed at all frequencies tested by 2 weeks after noise. Increased outer hair cell loss was also observed in Hsf1-/- mice following noise. These studies provide evidence for the importance of Hsf1 in cochlear protection, recovery, and/or repair following noise overstimulation.