Heat shock factor 1-deficient mice exhibit decreased recovery of hearing following noise overstimulation
Fairfield, Damon A.; Lomax, Margaret I.; Dootz, Gary A.; Chen, Shu; Galecki, Andrzej T.; Benjamin, Ivor J.; Dolan, David F.; Altschuler, Richard A.
2005-08-15
Citation
Fairfield, Damon A.; Lomax, Margaret I.; Dootz, Gary A.; Chen, Shu; Galecki, Andrzej T.; Benjamin, Ivor J.; Dolan, David F.; Altschuler, Richard A. (2005)."Heat shock factor 1-deficient mice exhibit decreased recovery of hearing following noise overstimulation." Journal of Neuroscience Research 81(4): 589-596. <http://hdl.handle.net/2027.42/48686>
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.Publisher
Wiley Subscription Services, Inc., A Wiley Company
ISSN
0360-4012 1097-4547
Other DOIs
PMID
15952177
Types
Article
URI
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15952177&dopt=citationMetadata
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