Ongoing production of sensory cells in the vestibular epithelium of the chick

Roberson, David F.; Weisleder, Pedro; Bohrer, Pamela S.; Rubel, Edwin W.

doi:10.1016/0378-5955(92)90149-h

Cited by 137 publications

(116 citation statements)

References 18 publications

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“…Different culture conditions, different aminoglycosides, and species differences could account for the discrepancy in hair cell survival. For example, chick vestibular hair cells have been estimated to live from ϳ1 to 15 weeks, whereas mammalian vestibular hair cells are capable of surviving for the entire lifetime of the animal (Roberson et al, 1992;Rubel et al, 1995;Kil et al, 1997;Goodyear et al, 1999;Stone et al, 1999;Wilkins et al, 1999). These observations suggest that the cell death pathway(s) in the avian vestibular organs may show some important differences from their mammalian counterparts.…”

Section: General Caspase Inhibitors Promote Hair Cell Survivalmentioning

confidence: 82%

“…We determined that both cycloheximide and caspase inhibitors promoted hair cell survival after aminoglycoside exposure. Also, the mature avian vestibular sensory epithelia exhibit a low, ongoing level of cell proliferation (Jørgensen and Mathiesen, 1988;Roberson et al, 1992;Kil et al, 1997;Wilkins et al, 1999), which is accompanied by a comparable rate of spontaneous hair cell death (Kil et al, 1997;Wilkins et al, 1999). It is not known, however, whether the loss of hair cells stimulates supporting cell proliferation or whether proliferation triggers the apoptotic cell death of hair cells.…”

Section: Abstract: Auditory; Hair Cell; Vestibular; Tissue Culture; mentioning

confidence: 99%

“…Several previous studies have demonstrated ongoing cell proliferation in mature vestibular organs (Jørgensen and Mathiesen, 1988;Roberson et al, 1992;Weisleder and Rubel, 1993;Rubel et al, 1995;Kil et al, 1997;Wilkins et al, 1999) and have demonstrated that the baseline level of proliferation appears to be counterbalanced by ongoing hair cell death (Kil et al, 1997;Goodyear et al, 1999;Stone et al, 1999;Wilkins et al, 1999). 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 .…”

Section: Relationship Between Spontaneous Hair Cell Death and Ongoingmentioning

confidence: 99%

“…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%

“…Hair cells in the mature avian vestibular system die spontaneously and are replaced continuously (Jørgensen and Mathiesen, 1988;Roberson et al, 1992;Kil et al, 1997;Wilkins et al, 1999). To characterize the amount of ongoing cell apoptosis in vestibular organs, we cultured utricles in control medium for 24 hr and then processed them for TUNEL labeling.…”

Section: Ongoing Cell Death Occurs In Cultured Utriclesmentioning

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: General Caspase Inhibitors Promote Hair Cell Survivalmentioning

confidence: 82%

Section: Abstract: Auditory; Hair Cell; Vestibular; Tissue Culture; mentioning

confidence: 99%

Section: Relationship Between Spontaneous Hair Cell Death and Ongoingmentioning

confidence: 99%

Section: Preventing Ongoing Cell Death Reduces Supporting Cell Prolifmentioning

confidence: 99%

Section: Ongoing Cell Death Occurs In Cultured Utriclesmentioning

confidence: 99%

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Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

2002

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Early ear development in the embryo of the Zebrafish,Danio rerio

1996

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The zebrafish provides an important model for vertebrate inner ear development. The otic placode becomes visible at approximately 16 hours (at 28.5 degrees C) and forms a vesicle with a lumen by cavitation at approximately 18 hours. Two otoliths appear in the lumen by 19.5 hours, and at about 24 hours the first sensory hair cells are seen, grouped in two small patches, one beneath each otolith, corresponding to future maculae. Staining with fluorescent phalloidin reveals 10-20 hair cells in each macula by 42 hours; between 3 days and 7 days the numbers grow to approximately 80 per macula. Neurons of the statoacoustic ganglion are first visible by staining with HNK-1 antibody at about 24 hours. Serial sections and time-lapse films show that the neuronal precursors originate by delamination from the ventral face of the otocyst; the peak period of delamination is from 22 hours to 30 hours. The system of semicircular canals forms between 42 hours and 72 hours by outgrowth of protrusions from the walls of the otocyst to form pillars of tissue spanning the lumen. Three further clusters of hair cells also become visible in this period, forming the three cristae. Thus, by the end of the first week, all key components of the ear are present. Subsequent growth produces thousands more hair cells; additional neurons probably derive from proliferation of neuronal precursors within the ganglion. Although the timetable is species-specific, the principles of inner ear development in the zebrafish seem to be the same as in other vertebrates.

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Induction of cell proliferation in avian inner ear sensory epithelia by insulin-like growth factor-I and insulin

1997

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Postembryonic production of inner-ear hair cells occurs both normally and after insult in lower vertebrates and avians. To determine how this proliferation is controlled, several growth factors were tested for effects on progenitor-cell division in cultured avian vestibular sensory epithelium. Mitogenic effects of bombesin, epidermal growth factor, insulin-like growth factor-I (IGF-I), insulin, and transforming growth factor-a were assayed in organotypic cultures of utricles from the mature, undamaged (normal) chicken inner ear. Tritiated thymidine and autoradiographic techniques and 5-bromo-28-deoxyuridine (BrdU) immunocytochemistry were used to identify cells synthesizing DNA. IGF-I stimulated DNA synthesis in the vestibular sensory receptor epithelium in a dose-dependent manner. DNA synthesis was also stimulated by insulin. These results suggest that stimulation of the IGF-I receptors by IGF-I or insulin binding stimulates cell proliferation in the mature avian vestibular sensory epithelium.

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Ongoing production of sensory cells in the vestibular epithelium of the chick

Cited by 137 publications

References 18 publications

Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

Early ear development in the embryo of the Zebrafish,Danio rerio

Induction of cell proliferation in avian inner ear sensory epithelia by insulin-like growth factor-I and insulin

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