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Heat shock factor 1‐deficient mice exhibit decreased recovery of hearing following noise overstimulation
Author(s) -
Fairfield Damon A.,
Lomax Margaret I.,
Dootz Gary A.,
Chen Shu,
Galecki Andrzej T.,
Benjamin Ivor J.,
Dolan David F.,
Altschuler Richard A.
Publication year - 2005
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20417
Subject(s) - hsf1 , cochlea , heat shock factor , noise induced hearing loss , stimulation , hearing loss , heat shock , heat shock protein , noise (video) , hair cell , medicine , biology , endocrinology , hsp70 , audiology , noise exposure , biochemistry , gene , artificial intelligence , computer science , image (mathematics)
Abstract 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.