Regeneration of Sensory Hair Cells After Acoustic Trauma

Corwin, Jeffrey T.; Cotanche, Douglas A.

doi:10.1126/science.3381100

Cited by 752 publications

(527 citation statements)

References 12 publications

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“…This dynamic pattern of ongoing cell death and proliferation differs from that observed in the chicken cochlea, in which the supporting cells are mitotically quiescent until the hair cells are lost because of trauma (Corwin and Cotanche, 1988; or proliferate at a very low rate . The results of these previous studies, however, leave the relationship between ongoing cell death and cell proliferation unclear.…”

Section: Relationship Between Spontaneous Hair Cell Death and Ongoingmentioning

confidence: 49%

“…It has been hypothesized that the death of hair cells triggers the proliferation of nearby supporting cells (Corwin and Cotanche, 1988;Girod et al, 1989;Raphael and Altschuler, 1992;Roberson et al, 1992;Hashino and Salvi, 1993;Stone and Cotanche, 1994;Warchol and Corwin, 1996). To investigate the relationship between ongoing cell death and the level of supporting cell proliferation in the chick vestibular organs, we inhibited hair cell death by treatment with BAF.…”

Section: Preventing Ongoing Cell Death Reduces Supporting Cell Prolifmentioning

confidence: 99%

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Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

2002

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Sensory hair cells die after acoustic trauma or ototoxic insults, but the signal transduction pathways that mediate hair cell death are not known. Here we identify several important signaling events that regulate the death of vestibular hair cells. Chick utricles were cultured in media supplemented with the ototoxic antibiotic neomycin and selected pharmacological agents that influence signaling molecules in cell death pathways. Hair cells that were treated with neomycin exhibited classically defined apoptotic morphologies such as condensed nuclei and fragmented DNA. Inhibition of protein synthesis (via treatment with cycloheximide) increased hair cell survival after treatment with neomycin, suggesting that hair cell death requires de novo protein synthesis. Finally, the inhibition of caspases promoted hair cell survival after neomycin treatment.Sensory hair cells in avian vestibular organs also undergo continual cell death and replacement throughout mature life. It is unclear whether the loss of hair cells stimulates the proliferation of supporting cells or whether the production of new cells triggers the death of hair cells. We examined the effects of caspase inhibition on spontaneous hair cell death in the chick utricle. Caspase inhibitors reduced the amount of ongoing hair cell death and ongoing supporting cell proliferation in a dosedependent manner. In isolated sensory epithelia, however, caspase inhibitors did not affect supporting cell proliferation directly. Our data indicate that ongoing hair cell death stimulates supporting cell proliferation in the mature utricle.

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Section: Relationship Between Spontaneous Hair Cell Death and Ongoingmentioning

confidence: 49%

Section: Preventing Ongoing Cell Death Reduces Supporting Cell Prolifmentioning

confidence: 99%

Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

2002

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“…There have been a number of studies describing cochlear pathology in birds as a result of acoustic overstimulation (Cotanche, 1987;Cotanche et al, 1987;Cotanche and Corwin, 1991;Cousillas and Rebillard, 1988;Corwin and Cotanche, 1988;Girod et al, 1989;Saunders et al, 1992) and ototoxicity of antibiotic drugs (Hashino et al, 1992;Hashino et al, 1991;Girod et al, 1991;Pickles and Rouse, 1991). We can thus compare the pathologies found in the cochlea of the Waterslagers with those observed in other birds after insult to the cochlea.…”

Section: /Hearing Research 79 (1994) 123-136 133mentioning

confidence: 99%

Inner-ear abnormalities and their functional consequences in Belgian Waterslager canaries (Serinus canarius)

Gleich

Dooling²,

Manley

1994

Hearing Research

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Recent reports of elevated auditory thresholds in canaries of the Belgian Waterslager strain have shown thai this strain has an inherited auditory deficit in which absolute auditory thresholds at high frequencies (i.e. above 2.(1 kHz) are as much as 41) dB less sensitive than the thresholds of mixed-breed canaries and those of other strains. The measurement of CAP audiograms showed that the hearing deficit is already present at the level of the auditory nerve (Gleich and Dooling, 1992). Here we show gross abnormalities in the anatomy of the basilar papilla of Belgian Waterslager canaries at the level of the hair cell. The extent of these abnormalities was correlated with the amount of hearing deficit as measured behaviorally.

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“…4 SCs perform many functions, including providing critical trophic factors, preventing excitotoxicity, and mediating regeneration in those systems (non-mammalian vertebrates) capable of replacing lost HCs. [5][6][7][8][9][10][11] When HCs die, SCs also preserve the integrity and function of the remaining tissue by forming scars and clearing dead HCs. 2,[12][13][14][15][16][17] Maintaining a fluid barrier at the surface of the sensory epithelium after damage is necessary to preserve the electro-chemical gradient that drives HC depolarization and therefore sensory transduction after the onset of hearing (reviewed in Wangemann).…”

mentioning

confidence: 99%

Live imaging the phagocytic activity of inner ear supporting cells in response to hair cell death

et al. 2015

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Hearing loss and balance disorders affect millions of people worldwide. Sensory transduction in the inner ear requires both mechanosensory hair cells (HCs) and surrounding glia-like supporting cells (SCs). HCs are susceptible to death from aging, noise overexposure, and treatment with therapeutic drugs that have ototoxic side effects; these ototoxic drugs include the aminoglycoside antibiotics and the antineoplastic drug cisplatin. Although both classes of drugs are known to kill HCs, their effects on SCs are less well understood. Recent data indicate that SCs sense and respond to HC stress, and that their responses can influence HC death, survival, and phagocytosis. These responses to HC stress and death are critical to the health of the inner ear. Here we have used live confocal imaging of the adult mouse utricle, to examine the SC responses to HC death caused by aminoglycosides or cisplatin. Our data indicate that when HCs are killed by aminoglycosides, SCs efficiently remove HC corpses from the sensory epithelium in a process that includes constricting the apical portion of the HC after loss of membrane integrity. SCs then form a phagosome, which can completely engulf the remaining HC body, a phenomenon not previously reported in mammals. In contrast, cisplatin treatment results in accumulation of dead HCs in the sensory epithelium, accompanied by an increase in SC death. The surviving SCs constrict fewer HCs and display impaired phagocytosis. These data are supported by in vivo experiments, in which cochlear SCs show reduced capacity for scar formation in cisplatin-treated mice compared with those treated with aminoglycosides. Together, these data point to a broader defect in the ability of the cisplatin-treated SCs, to preserve tissue health in the mature mammalian inner ear. . 4 SCs perform many functions, including providing critical trophic factors, preventing excitotoxicity, and mediating regeneration in those systems (non-mammalian vertebrates) capable of replacing lost HCs. 5-11 When HCs die, SCs also preserve the integrity and function of the remaining tissue by forming scars and clearing dead HCs. 2,12-17 Maintaining a fluid barrier at the surface of the sensory epithelium after damage is necessary to preserve the electro-chemical gradient that drives HC depolarization and therefore sensory transduction after the onset of hearing (reviewed in Wangemann). 18 Several major stressors cause HC death, 19-22 including aging, noise trauma, and exposure to therapeutic drugs with ototoxic side effects. When a HC is killed by noise or aminoglycoside antibiotics, surrounding SCs form a filamentous actin (F-actin) cable that constricts the HC at its apex. 2,[12][13][14][15][16][17] This process separates the apical portion of the cell, including the stereocilia bundle, from the HC body and preserves a sealed reticular lamina. 23 In the chick utricle, following the apical constriction of dead HCs, the SCs engulf and phagocytose the remaining HC corpse. 15 Additional data from the chick indicate that the ototoxi...

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Regeneration of Sensory Hair Cells After Acoustic Trauma

Cited by 752 publications

References 12 publications

Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

Inner-ear abnormalities and their functional consequences in Belgian Waterslager canaries (Serinus canarius)

Live imaging the phagocytic activity of inner ear supporting cells in response to hair cell death

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