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

dc.contributor.authorFairfield, Damon A.en_US
dc.contributor.authorLomax, Margaret I.en_US
dc.contributor.authorDootz, Gary A.en_US
dc.contributor.authorChen, Shuen_US
dc.contributor.authorGalecki, Andrzej T.en_US
dc.contributor.authorBenjamin, Ivor J.en_US
dc.contributor.authorDolan, David F.en_US
dc.contributor.authorAltschuler, Richard A.en_US
dc.date.accessioned2006-09-20T15:01:54Z
dc.date.available2006-09-20T15:01:54Z
dc.date.issued2005-08-15en_US
dc.identifier.citationFairfield, 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.issn0360-4012en_US
dc.identifier.issn1097-4547en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/48686
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15952177&dopt=citationen_US
dc.description.abstractHeat 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.extent316904 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology and Psychiatryen_US
dc.titleHeat shock factor 1-deficient mice exhibit decreased recovery of hearing following noise overstimulationen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelPsychologyen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.subject.hlbtoplevelSocial Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumKresge 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, Michiganen_US
dc.contributor.affiliationumKresge 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, Michiganen_US
dc.contributor.affiliationumKresge Hearing Research Institute, Department of Otolaryngology/Head Neck Surgery, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumInstitute of Gerontology, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumInstitute of Gerontology, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumKresge Hearing Research Institute, Department of Otolaryngology/Head Neck Surgery, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumKresge 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 48109-0506en_US
dc.contributor.affiliationotherDepartment of Internal Medicine, Division of Cardiology, University of Utah, Salt Lake City, Utahen_US
dc.identifier.pmid15952177en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/48686/1/20417_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/jnr.20417en_US
dc.identifier.sourceJournal of Neuroscience Researchen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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