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- W2023598703 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." @default.
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- W2023598703 date "2005-08-15" @default.
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- W2023598703 title "Heat shock factor 1-deficient mice exhibit decreased recovery of hearing following noise overstimulation" @default.
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- W2023598703 doi "https://doi.org/10.1002/jnr.20417" @default.
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