Temporal and genetic influences on protection against noise-induced hearing loss by hypoxic preconditioning in mice

Gagnon, Patricia M.; Simmons, Dwayne D.; Bao, Jianxin; Lei, Debin; Ortmann, Amanda; Ohlemiller, Kevin K.

doi:10.1016/j.heares.2006.09.006

Cited by 25 publications

(29 citation statements)

References 53 publications

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“…The phenomenon of conditioning originally referred to protection induced by preexposure to moderate-level (nontraumatic) sound (Canlon et al, 1988; Campo et al, 1991; Ryan et al, 1994; Niu and Canlon, 2002), but a variety of stimuli have been found to induce conditioning, including restraint stress (Wang and Liberman, 2002; Tahera et al, 2006b), heat stress (Yoshida et al, 1999), sham surgery (Kujawa and Liberman, 1997), corticosteroids (Takemura et al, 2004; Tabuchi et al, 2006; Tahera et al, 2006b), kanamycin (Fernandez et al, 2010), and hypoxia (Gagnon et al, 2007). Indeed, Wang and Liberman (2002) suggested that it is the stress that results from exposure to the acoustic conditioning procedure, rather than the acoustic signal itself, that may underlie the protection.…”

Section: Discussionmentioning

confidence: 99%

A Corticosteroid-Responsive Transcription Factor, Promyelocytic Leukemia Zinc Finger Protein, Mediates Protection of the Cochlea from Acoustic Trauma

Peppi¹,

Kujawa²,

Sewell³

2011

J. Neurosci.

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Animals can be induced to resist cochlear damage associated with acoustic trauma by exposure to a variety of “conditioning” stimuli, including restraint stress, moderate level sound, heat stress, hypoxia, and corticosteroids. Here we identify in mice a corticosteroid-responsive transcription factor, PLZF (promyelocytic leukemia zinc finger protein), which mediates conditioned protection of the cochlea from acoustic trauma. PLZF mRNA levels in the cochlea are increased following conditioning stimuli, including restraint stress, dexamethasone administration, and moderate-to-high level acoustic stimulation. Heterozygous mutant (luxoid.Zbtb16LU/J) mice deficient in PLZF have hearing and responses to acoustic trauma similar to their wild type littermates but are unable to generate conditioning-induced protection from acoustic trauma. PLZF immunoreactivity is present in the spiral ganglion, lateral wall of the cochlea, and organ of Corti, all targets for acoustic trauma. PLZF is also present in the brain and PLZF mRNA in brain is elevated following conditioning stimuli. The identification of a transcription factor that mediates conditioned protection from trauma provides a tool for understanding the protective action of corticosteroids, which are widely used in treating acute hearing loss, and has relevance to understanding the role of corticosteroids in trauma protection.

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Section: Discussionmentioning

confidence: 99%

A Corticosteroid-Responsive Transcription Factor, Promyelocytic Leukemia Zinc Finger Protein, Mediates Protection of the Cochlea from Acoustic Trauma

Peppi¹,

Kujawa²,

Sewell³

2011

J. Neurosci.

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“…Genetic analysis of Hif function in multiple species and the developmental defects in Hif-deficient embryos have revealed the importance of oxygen availability and Hif as a key regulator of ontogeny (Simon and Keith, 2008). In another report, the protective benefits of hypoxic preconditioning against permanent noiseinduced hearing loss (NIHL) shown in CBA mice were associated with significant upregulation of Hif-1a within the organ of Corti (Gagnon et al, 2007). Accordingly, these evidences implicate a great survival promotion benefit of Hif-1a in response to hypoxia stimulation, although the mechanisms regulating cochlear SPC behavior via Hif have yet to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia enhances the stemness markers of cochlear stem/progenitor cells and expands sphere formation through activation of hypoxia-inducible factor-1alpha

et al. 2011

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“…Preconditioning refers to a mildly injurious event that confers protection against a later, more injurious, event (Gidday 2006;Dirnagl et al 2003;Eisen et al 2004;Ran et al 2005). Demonstrated preconditioning inducers against NIPTS in mice include mild noise, heat stress, restraint, and hypoxia (Yoshida et al 1999;Wang and Liberman 2002;Yoshida and Liberman 2000;Niu and Canlon 2002;Gagnon et al 2007). Two studies have reported partial protection in guinea pigs by amikacin or gentamicin against later, high-dose, application of the same ototoxins (De Oliveira et al 2004;Maudonnet et al 2008).…”

Section: Sub-chronic Kanamycin As a Form Of Preconditioningmentioning

confidence: 99%

Protection against Noise-Induced Hearing Loss in Young CBA/J Mice by Low-Dose Kanamycin

Fernandez

Ohlemiller

Gagnon

et al. 2010

JARO

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Animal studies indicate that a combination of kanamycin (KM) and noise produces a synergistic effect, whereby the threshold shift from the combination is greater than the sum of the shifts caused by either agent alone. Most such studies have focused on adult animals, and it has remained unclear whether younger, presumably more susceptible, animals show an even greater synergistic effect. The present study tested the hypothesis that young CBA/J mice receiving a low dose of KM (300 mg/kg, 2×/day, s.c.) from 20 to 30 days post-gestational age followed by brief noise exposure (110 dB SPL; 4-45 kHz, 30 s) would show greater noise-induced permanent threshold shifts (NIPTS) than mice receiving either treatment alone. Noise exposure produced 30-40 dB of NIPTS and moderate hair cell loss in young saline-treated mice. KM alone at this dose had no effect on thresholds. Surprisingly, mice receiving KM plus noise were protected from NIPTS, showing ABR thresholds not significantly different from unexposed controls. Mice receiving KM prior to noise exposure also showed significantly less outer hair cell loss than saline-treated mice. Additional experiments indicated protection by KM when the noise was applied either 24 or 48 h after the last KM injection. Our results demonstrate a powerful protective effect of subchronic low-dose kanamycin against NIPTS in young CBA/J mice. Repeated kanamycin exposure may establish a preconditioned protective state, the molecular bases of which remain to be determined.

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Temporal and genetic influences on protection against noise-induced hearing loss by hypoxic preconditioning in mice

Cited by 25 publications

References 53 publications

A Corticosteroid-Responsive Transcription Factor, Promyelocytic Leukemia Zinc Finger Protein, Mediates Protection of the Cochlea from Acoustic Trauma

A Corticosteroid-Responsive Transcription Factor, Promyelocytic Leukemia Zinc Finger Protein, Mediates Protection of the Cochlea from Acoustic Trauma

Hypoxia enhances the stemness markers of cochlear stem/progenitor cells and expands sphere formation through activation of hypoxia-inducible factor-1alpha

Protection against Noise-Induced Hearing Loss in Young CBA/J Mice by Low-Dose Kanamycin

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