Portal de Periódicos da CAPES

Heat shock factor 1-deficient mice exhibit decreased recovery of hearing following noise overstimulation

2005; Wiley; Volume: 81; Issue: 4 Linguagem: Inglês

10.1002/jnr.20417

1097-4547

Damon A. Fairfield, Margaret I. Lomax, Gary A. Dootz, Shu Chen, Andrzej T. Gałecki, Ivor J. Benjamin, David F. Dolan, Richard A. Altschuler,

Connexins and lens biology

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. © 2005 Wiley-Liss, Inc.