Heat shock factor 1-deficient mice exhibit decreased recovery of hearing following noise overstimulation
dc.contributor.author | Fairfield, Damon A. | en_US |
dc.contributor.author | Lomax, Margaret I. | en_US |
dc.contributor.author | Dootz, Gary A. | en_US |
dc.contributor.author | Chen, Shu | en_US |
dc.contributor.author | Galecki, Andrzej T. | en_US |
dc.contributor.author | Benjamin, Ivor J. | en_US |
dc.contributor.author | Dolan, David F. | en_US |
dc.contributor.author | Altschuler, Richard A. | en_US |
dc.date.accessioned | 2006-09-20T15:01:54Z | |
dc.date.available | 2006-09-20T15:01:54Z | |
dc.date.issued | 2005-08-15 | en_US |
dc.identifier.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> | en_US |
dc.identifier.issn | 0360-4012 | en_US |
dc.identifier.issn | 1097-4547 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/48686 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15952177&dopt=citation | en_US |
dc.description.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. | en_US |
dc.format.extent | 316904 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Neuroscience, Neurology and Psychiatry | en_US |
dc.title | Heat shock factor 1-deficient mice exhibit decreased recovery of hearing following noise overstimulation | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbsecondlevel | Psychology | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Social Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Kresge Hearing Research Institute, Department of Otolaryngology/Head Neck Surgery, University of Michigan, Ann Arbor, Michigan ; Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Kresge Hearing Research Institute, Department of Otolaryngology/Head Neck Surgery, University of Michigan, Ann Arbor, Michigan ; Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Kresge Hearing Research Institute, Department of Otolaryngology/Head Neck Surgery, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Institute of Gerontology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Institute of Gerontology, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Kresge Hearing Research Institute, Department of Otolaryngology/Head Neck Surgery, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Kresge Hearing Research Institute, Department of Otolaryngology/Head Neck Surgery, University of Michigan, Ann Arbor, Michigan ; Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan ; KHRI, Department of Otolaryngology, The University of Michigan, 1301 East Ann Street, Ann Arbor, MI 48109-0506 | en_US |
dc.contributor.affiliationother | Department of Internal Medicine, Division of Cardiology, University of Utah, Salt Lake City, Utah | en_US |
dc.identifier.pmid | 15952177 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/48686/1/20417_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/jnr.20417 | en_US |
dc.identifier.source | Journal of Neuroscience Research | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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