Sound Needs Sound Melanocytes to Be Heard

Tachibana, Masayoshi

doi:10.1111/j.1600-0749.1999.tb00518.x

Cited by 119 publications

(121 citation statements)

References 80 publications

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“…Melanocytes also populate vestibular regions and the endolymphatic apparatus in the mammalian ear (Masuda et al, 1994;Escobar et al, 1995;Peters et al, 1995;Stanchina et al, 2006), but their role here is less clear; for example, mutations in Kcnj10 have no effect on vestibular endolymph (Marcus et al, 2002). Analysis of the inner ear phenotype in murine models of WS and other auditory-pigmentary disorders has focused on the presence of intermediate cells in the stria vascularis; deafness is usually attributed to the loss of intermediate cells in this tissue, leading to a reduction or collapse of endolymph volume, a loss of the endocochlear potential and subsequent hair cell degeneration (Tachibana et al, 1992;Cable et al, 1994;Matsushima et al, 2002;Stanchina et al, 2006) (reviewed by Tachibana, 1999;Tachibana et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…In mammals, neural-crest-derived melanocytes populate the stria vascularis of the cochlea as intermediate cells. These are thought to play a protective role and are essential for both the maintenance of endolymph composition and generation of the endocochlear potential (Steel and Barkway, 1989;Cable et al, 1992;Cable et al, 1993;Cable et al, 1994) (reviewed by Steel, 1995;Tachibana, 1999;Price and Fisher, 2001;Wangemann, 2002;Wangemann, 2006;Lang et al, 2007). In the mouse, maintenance of the endocochlear potential depends on expression of the potassium channel Kcnj10 in intermediate cells (Marcus et al, 2002;Wangemann et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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A zebrafish model for Waardenburg syndrome type IV reveals diverse roles for Sox10 in the otic vesicle

Dutton

Abbas

Spencer

et al. 2009

Disease Models &Amp; Mechanisms

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SUMMARYIn humans, mutations in the SOX10 gene are a cause of the auditory-pigmentary disorder Waardenburg syndrome type IV (WS4) and related variants. SOX10 encodes an Sry-related HMG box protein essential for the development of the neural crest; deafness in WS4 and other Waardenburg syndromes is usually attributed to loss of neural-crest-derived melanocytes in the stria vascularis of the cochlea. However, SOX10 is strongly expressed in the developing otic vesicle and so direct roles for SOX10 in the otic epithelium might also be important. Here, we examine the otic phenotype of zebrafish sox10 mutants, a model for WS4. As a cochlea is not present in the fish ear, the severe otic phenotype in these mutants cannot be attributed to effects on this tissue. In zebrafish sox10 mutants, we see abnormalities in all otic placodal derivatives. Gene expression studies indicate deregulated expression of several otic genes, including fgf8, in sox10 mutants. Using a combination of mutant and morphant data, we show that the three sox genes belonging to group E (sox9a, sox9b and sox10) provide a link between otic induction pathways and subsequent otic patterning: they act redundantly to maintain sox10 expression throughout otic tissue and to restrict fgf8 expression to anterior macula regions. Single-cell labelling experiments indicate a small and transient neural crest contribution to the zebrafish ear during normal development, but this is unlikely to account for the strong defects seen in the sox10 mutant. We discuss the implication that the deafness in WS4 patients with SOX10 mutations might reflect a haploinsufficiency for SOX10 in the otic epithelium, resulting in patterning and functional abnormalities in the inner ear.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A zebrafish model for Waardenburg syndrome type IV reveals diverse roles for Sox10 in the otic vesicle

Dutton

Abbas

Spencer

et al. 2009

Disease Models &Amp; Mechanisms

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“…Increasing amounts of UV-light, meaning increasing doses of sunlight, causes the melanocytes to increase their production of melanin. Melanocytes also produce pigment for the hair follicles, and they are also present in the cochlea (Tachibana, 1999;Uehara et al, 2009), brain (Goldgeier et al, 1984;, and adipose tissue ) and several other sites 10 . e retinal pigment epithelium of the eyes is also made up of another pigment-producing cell type .…”

Section: Melanocytes and Pigmentationmentioning

confidence: 99%

Fibroblast Differentiation and Models of Human Skin

Rakar¹

2016

Linköping University Medical Dissertations

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Denna bok avhandlar en riktning av biomedicinsk forskning som i det långa loppet sy ar till att nå bättre och banbrytande sätt att läka våra kroppar. Forskningen vilar på en tredelad grund -viktiga kunskaper som leder mot en generell förståelse för hur celler blir till vävnader, hur vävnad-er och organ kan manipuleras på ett kliniskt användbart sätt, och till sist hur denna kunskap kan appliceras på människans hudorgan.Den första delen handlar om cellers identitet, och den stora potentialen som våra egna stamceller har för framtidens läkekonst. Genom att förstå hur celler egentligen fungerar på arvsmassenivå kan vi utöka arsenalen av verktyg vi har för att få celler att bete sig på de sätt som behövs för att skapa nya organ. Vi har jobbat med att karakterisera och manipulera broblaster, en av de vanligaste celltyperna i människokroppen, och bland annat tagit fram olika typer av fettceller.Den andra delen handlar om hur man använder celler, biokemiska faktorer och biokompatibla material för att konstruera vävnader och organ. Innan forskningen når klinisk användbarhet har vi möjlighet att bygga begränsade modellsystem för att studera människans biologi. Cellsystem på labbet är mycket viktiga verktyg för att föra forskningen på vävnadsbyg-gande framåt.Den tredje delen behandlar hudforskning speci kt, och här samlas kunskaper från tidigare delarna som är relevanta för mänsklig hud. Här beskrivs användningen av två olika hudmodeller för att undersöka proceser viktiga vid sårläkning. Vidare beskrivs planerna kring ett större påbörjat projekt som sy ar till att använda alla tidigare lärdomar och tekniker för att åstadkomma en ny terapi för sårläkning.Abstract is thesis combines three publications and one manuscript, covering two principal topics: functional di erentiation of human broblasts and, laboratory models of human skin. e two topics favourably unite in the realm of tissue engineering. is thesis is therefore split into three main parts: 1. a discussion of phenotypic plasticity as it pertains to broblasts and the stem cell continuum; 2. a short review of engineered tissue, with particular focus on soluble factors and materials; and, 3. a motivated review of the biology, diversity and culture of skin, including skin construction. e intended goal of our research endeavor was to achieve the formulation of a bioactive therapy for skin regeneration. e main hypothesis was that broblast-to-keratinocyte di erentiation would facilitate wound healing, and that the protocol for such a method could be adapted to clinical translation. e foundation for the hypothesis lay in the di erentiation capabilities of primary dermal broblasts (Paper I). However, the goal has not yet been achieved. Instead, intermediate work on the construction of skin for the purpose of creating a model test-bed has resulted in two other publications. e use of excised human skin, a formidable reference sample for tissue engineered skin, has been used to investigate a gelatin-based material in re-epithelialization (Paper II). A rst attempt at standardizi...

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“…It has been demonstrated that the high throughput of K ϩ across ICs membrane yields EP (14,52,53). A combination of immunohistochemistry (16,54), pharmacological (44), and null mutant mice experiments (17) have resulted in the assertion that Kir4.1 channels residing at membranes of intermediate cells in the StV confer the extrusion of K ϩ to polarize the membrane.…”

Section: Kir41 In the Inner Earmentioning

confidence: 99%

Functional Consequences of Polyamine Synthesis Inhibition by l-α-Difluoromethylornithine (DFMO)

Nie

Feng

Diaz

et al. 2005

Journal of Biological Chemistry

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L-␣-Difluoromethylornithine (DFMO) is a chemopreventive agent for colon cancer in clinical trials. Yet, the drug produces an across-frequency elevation of the hearing threshold, suggesting that DFMO may affect a common trait along the cochlear spiral. The mechanism for the ototoxic effects of DFMO remains uncertain. The cochlear duct is exclusively endowed with endocochlear potential (EP). EP is a requisite for normal sound transduction, as it provides the electromotive force that determines the magnitude of the receptor potential of hair cells. EP is generated by the high throughput of K ؉ across cells of the stria vascularis, conferred partly by the activity of Kir4.1 channels. Here, we show that the ototoxicity of DFMO may be mediated by alteration of the inward rectification of Kir4.1 channels, resulting in a marked reduction in EP. These findings are surprising given that the present model for EP generation asserts that Kir4.1 confers the outflow of K ؉ in the stria vascularis. We have proposed an alternative model. These findings should also enable the rational design of new pharmaceuticals devoid of the untoward effect of DFMO.

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Sound Needs Sound Melanocytes to Be Heard

Cited by 119 publications

References 80 publications

A zebrafish model for Waardenburg syndrome type IV reveals diverse roles for Sox10 in the otic vesicle

A zebrafish model for Waardenburg syndrome type IV reveals diverse roles for Sox10 in the otic vesicle

Fibroblast Differentiation and Models of Human Skin

Functional Consequences of Polyamine Synthesis Inhibition by l-α-Difluoromethylornithine (DFMO)

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