Hair cell recovery in the vestibular sensory epithelia of mature guinea pigs

Forge, Andrew; Li, Lin; Nevill, Graham

doi:10.1002/(sici)1096-9861(19980720)397:1<69::aid-cne6>3.3.co;2-v

Cited by 132 publications

(12 citation statements)

References 12 publications

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“…In normal mice older than 6 weeks, Type I and II hair cells are removed from the utricle by supporting cells, which act like resident phagocytes, and Type II hair cells (but not Type I hair cells) are replaced by supporting cells (Bucks et al, 2017). Similar hair cell turnover appears to occur in bats (Kirkegaard & Jørgensen, 2000;Kirkegaard & Jørgensen, 2001) and guinea pigs (Forge et al, 1993(Forge et al, , 1998Lambert, Gu, & Corwin, 1997).…”

Section: Identity and Positioning Of Neonatally-added Hair Cellsmentioning

confidence: 89%

“…However, the morphology and innervation of Type I and Type II hair cells do not mature until P14-P17. In contrast to the neighboring cochlea, this elongated period of development correlates with the increased plasticity of the adult Density of tdTomato-positive hair cells labeled with different markers in Plp-CreER T2 :Rosa26 tdTomato mice at P30 (28 days posttamoxifen) utricle, where both turnover (Bucks et al, 2017) and spontaneous hair cell regeneration (Bucks et al, 2017;Forge et al, 1993Forge et al, , 1998Golub et al, 2012;Kawamoto et al, 2009) can occur.…”

Section: Identity and Positioning Of Neonatally-added Hair Cellsmentioning

confidence: 99%

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Development of hair cell phenotype and calyx nerve terminals in the neonatal mouse utricle

Warchol

Massoodnia

Pujol

et al. 2019

J of Comparative Neurology

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The vestibular organs of reptiles, birds, and mammals possess Type I and Type II sensory hair cells, which have distinct morphologies, physiology, and innervation. Little is known about how vestibular hair cells adopt a Type I or Type II identity or acquire proper innervation. One distinguishing marker is the transcription factor Sox2, which is expressed in all developing hair cells but persists only in Type II hair cells in maturity. We examined Sox2 expression and formation of afferent nerve terminals in mouse utricles between postnatal days 0 (P0) and P17. Between P3 and P14, many hair cells lost Sox2 immunoreactivity and the density of calyceal afferent nerve terminals (specific to Type I hair cells) increased in all regions of the utricle. At early time points, many calyces enclosed Sox2‐labeled hair cells, while some Sox2‐negative hair cells within the striola had not yet developed a calyx. These observations indicate that calyx maturation is not temporally correlated with loss of Sox2 expression in Type I hair cells. To determine which type(s) of hair cells are formed postnatally, we fate‐mapped neonatal supporting cells by injecting Plp‐CreER T2:Rosa26 tdTomato mice with tamoxifen at P2 and P3. At P9, tdTomato‐positive hair cells were immature and not classifiable by type. At P30, tdTomato‐positive hair cells increased 1.8‐fold compared to P9, and 91% of tdTomato‐labeled hair cells were Type II. Our findings show that most neonatally‐derived hair cells become Type II, and many Type I hair cells (formed before P2) downregulate Sox2 and acquire calyces between P0 and P14.

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Section: Identity and Positioning Of Neonatally-added Hair Cellsmentioning

confidence: 89%

Section: Identity and Positioning Of Neonatally-added Hair Cellsmentioning

confidence: 99%

Development of hair cell phenotype and calyx nerve terminals in the neonatal mouse utricle

Warchol

Massoodnia

Pujol

et al. 2019

J of Comparative Neurology

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“…Here, damage to hair cells, involved in balance and hearing, triggers the direct conversion of neighboring glial-like supportive cells to new hair cells. (Bramhall, Shi, Arnold, Hochedlinger, & Edge, 2014;Cox et al, 2014;Forge, Li, & Nevill, 1998;Mizutari et al, 2013;Richardson & Atkinson, 2015). In the liver also, damage to biliary epithelial cells sparks the reprogramming of surrounding hepatocytes to form new biliary epithelial cells (reviewed in Eberhard & Tosh, 2008;Yanger et al, 2013).…”

Section: Adaptive Cellular Reprogrammingmentioning

confidence: 99%

Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves

Jessen

Arthur‐Farraj

2019

Glia

265

260

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Schwann cells respond to nerve injury by cellular reprogramming that generates cells specialized for promoting regeneration and repair. These repair cells clear redundant myelin, attract macrophages, support survival of damaged neurons, encourage axonal growth, and guide axons back to their targets. There are interesting parallels between this response and that found in other tissues. At the cellular level, many other tissues also react to injury by cellular reprogramming, generating cells specialized to promote tissue homeostasis and repair. And at the molecular level, a common feature possessed by Schwann cells and many other cells is the injury‐induced activation of genes associated with epithelial–mesenchymal transitions and stemness, differentiation states that are linked to cellular plasticity and that help injury‐induced tissue remodeling. The number of signaling systems regulating Schwann cell plasticity is rapidly increasing. Importantly, this includes mechanisms that are crucial for the generation of functional repair Schwann cells and nerve regeneration, although they have no or a minor role elsewhere in the Schwann cell lineage. This encourages the view that selective tools can be developed to control these particular cells, amplify their repair supportive functions and prevent their deterioration. In this review, we discuss the emerging similarities between the injury response seen in nerves and in other tissues and survey the transcription factors, epigenetic mechanisms, and signaling cascades that control repair Schwann cells, with emphasis on systems that selectively regulate the Schwann cell injury response.

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“…Mammalian auditory epithelium, composed of hair cells and supporting cells, has limited capability for regeneration, which remains an obstacle for the development of therapeutics for sensorineural hearing loss (Roberson & Rubel 1994;Forge et al 1998;White et al 2006). In contrast, in the avian auditory epithelium, the loss of hair cells leads to re-entry of supporting cells into the cell cycle, giving rise to both hair cells and supporting cells (Corwin & Cotanche 1988;Ryals & Rubel 1988).…”

Section: Growth Arrest In Postmitotic Mature Cellsmentioning

confidence: 99%

Extra‐cell cycle regulatory functions of cyclin‐dependent kinases (CDK) and CDK inhibitor proteins contribute to brain development and neurological disorders

2013

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In developing brains, neural progenitors exhibit cell cycle-dependent nuclear movement within the ventricular zone [interkinetic nuclear migration (INM)] and actively proliferate to produce daughter progenitors and/or neurons, whereas newly generated neurons exit from the cell cycle and begin pial surface-directed migration and maturation. Dysregulation of the balance between the proliferation and the cell cycle exit in neural progenitors is one of the major causes of microcephaly (small brain). Recent studies indicate that cell cycle machinery influences not only the proliferation but also INM in neural progenitors. Furthermore, several cell cycle-related proteins, including p27kip1, p57kip2, Cdk5, and Rb, regulate the migration of neurons in the postmitotic state, suggesting that the growth arrest confers dual functions on cell cycle regulators. Consistently, several types of microcephaly occur in conjunction with neuronal migration disorders, such as periventricular heterotopia and lissencephaly. However, cell cycle re-entry by disturbance of growth arrest in mature neurons is thought to trigger neuronal cell death in Alzheimer's disease. In this review, we introduce the cell cycle protein-mediated regulation of two types of nuclear movement, INM and neuronal migration, during cerebral cortical development, and discuss the roles of growth arrest in cortical development and neurological disorders.

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Hair cell recovery in the vestibular sensory epithelia of mature guinea pigs

Cited by 132 publications

References 12 publications

Development of hair cell phenotype and calyx nerve terminals in the neonatal mouse utricle

Development of hair cell phenotype and calyx nerve terminals in the neonatal mouse utricle

Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves

Extra‐cell cycle regulatory functions of cyclin‐dependent kinases (CDK) and CDK inhibitor proteins contribute to brain development and neurological disorders

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