Proliferation of vertebrate inner ear supporting cells

Wilkins, Heather R.; Presson, Joelle C.; Popper, Arthur N.

doi:10.1002/(sici)1097-4695(19990615)39:4<527::aid-neu6>3.0.co;2-k

Cited by 30 publications

(26 citation statements)

References 30 publications

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“…Spontaneous death of mature hair cells in cultures of inner ear sensory organs has been reported in previous studies Stone et al, 1996;Quint et al, 1998;Matsui et al, 2000a). In addition, avian vestibular hair cells have a relatively short lifespan (Kil et al, 1997;Goodyear et al, 1999;Stone et al, 1999;Wilkins et al, 1999), and this could be a causative agent for the density differences. Alternatively, the sensory epithelia could expand after placement in culture.…”

Section: Aminoglycosides Kill Vestibular Hair Cells In Vitromentioning

confidence: 73%

“…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: 94%

“…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%

“…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%

“…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: 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: Aminoglycosides Kill Vestibular Hair Cells In Vitromentioning

confidence: 73%

Section: Relationship Between Spontaneous Hair Cell Death and Ongoingmentioning

confidence: 94%

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

confidence: 99%

Section: Ongoing Cell Death Occurs In Cultured Utriclesmentioning

confidence: 99%

Section: General Caspase Inhibitors Promote Hair Cell Survivalmentioning

confidence: 99%

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Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

2002

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cProx1 immunoreactivity distinguishes progenitor cells and predicts hair cell fate during avian hair cell regeneration

Stone

Shang

Tomarev

2004

Developmental Dynamics

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Direct transdifferentiation gives rise to the earliest new hair cells in regenerating avian auditory epithelium

Roberson

Alosi

Cotanche

2004

J of Neuroscience Research

156

183

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The avian auditory epithelium is capable of complete regeneration after hair cell (HC) loss. Most new HCs arise via cell division, but approximately one-third of new HCs arise via direct transdifferentiation (DT), in which supporting cells (SCs) alter their phenotype without dividing. In this study, we used synchronous, gentamicin-induced near-total HC loss in the basal end of the epithelium and continuous infusion of the cell division marker bromodeoxyuridine (BrdU) to identify the origin of each individual regenerating HC. Early new HCs were identified by immunolabeling for the HC-specific marker myosin-VIIa, and mitotic cells with BrdU immunolabeling. The first new HCs arising via DT appear 72-96 hr after gentamicin, 24-48 hr earlier than the first new mitotic HCs. After Day 6, however, most new HCs are mitotic. The "intermediate" morphology that has been suggested to be characteristic of DT is seen in HCs arising via both pathways. These findings suggest that DT is a simpler, more rapid process that produces the first new HCs, and that mitotic regeneration is somewhat slower but ultimately produces most new HCs. The identical morphology of regenerating HCs from both pathways suggests that once HC fate is established, all new HCs follow similar cellular processes during differentiation and reorganization into the regenerated epithelium.

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Proliferation of vertebrate inner ear supporting cells

Cited by 30 publications

References 30 publications

Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

Inhibition of Caspases Prevents Ototoxic and Ongoing Hair Cell Death

cProx1 immunoreactivity distinguishes progenitor cells and predicts hair cell fate during avian hair cell regeneration

Direct transdifferentiation gives rise to the earliest new hair cells in regenerating avian auditory epithelium

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