ArticleThe Journal of biological chemistry2011
Partial requirement of endothelin receptor B in spiral ganglion neurons for postnatal development of hearing.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- A Systematic Review of Genes Affecting Endocochlear Potential.Journal of the Association for Research in Otolaryngology : JARO · 2026Pooled it
- EDNRB2 regulates fate, migration, and maturation of hair cell precursors in regenerating avian auditory epithelium explants.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cochlear Implantation Outcomes in Genotyped Subjects with Sensorineural Hearing Loss.Journal of the Association for Research in Otolaryngology : JARO · 2025Article
- Placode and neural crest origins of congenital deafness in mouse models of Waardenburg-Shah syndrome.iScience · 2025Article
- G protein-coupled receptors in cochlea: Potential therapeutic targets for hearing loss.Frontiers in molecular neuroscience · 2022Review
- Structural heart defects associated with ETBMC cardiovascular disorders · 2021Article
- Brain size reductions associated with endothelin B receptor mutation, a cause of Hirschsprung's disease.BMC neuroscience · 2021Article
- Transcriptomic analysis and ednrb expression in cochlear intermediate cells reveal developmental differences between inner ear and skin melanocytes.Pigment cell & melanoma research · 2021Article
- Single-Cell RNA-Seq of Cisplatin-Treated Adult Stria Vascularis Identifies Cell Type-Specific Regulatory Networks and Novel Therapeutic Gene Targets.Frontiers in molecular neuroscience · 2021Article
- Multidisciplinary approach to assess the toxicities of arsenic and barium in drinking water.Environmental health and preventive medicine · 2020Review
- Growth factor and receptor malfunctions associated with human genetic deafness.Clinical genetics · 2020Review
- Hearing impairments caused by genetic and environmental factors.Environmental health and preventive medicine · 2013Review
- c-Ret-mediated hearing losses.International journal of clinical and experimental pathology · 2012Review
- Molecular Network Associated with MITF in Skin Melanoma Development and Progression.Journal of skin cancer · 2011Article
- Loss-of-function mutation of c-Ret causes cerebellar hypoplasia in mice with Hirschsprung disease and Down's syndrome.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impairments of endothelin receptor B (Ednrb/EDNRB) cause the development of Waardenburg-Shah syndrome with congenital hearing loss, hypopigmentation, and megacolon disease in mice and humans. Hearing loss in Waardenburg-Shah syndrome has been thought to be caused by an Ednrb-mediated congenital defect of melanocytes in the stria vascularis (SV) of inner ears. Here we show that Ednrb expressed in spiral ganglion neurons (SGNs) in inner ears is required for postnatal development of hearing in mice. Ednrb protein was expressed in SGNs from WT mice on postnatal day 19 (P19), whereas it was undetectable in SGNs from WT mice on P3. Correspondingly, Ednrb homozygously deleted mice (Ednrb(-/-) mice) with congenital hearing loss showed degeneration of SGNs on P19 but not on P3. The congenital hearing loss involving neurodegeneration of SGNs as well as megacolon disease in Ednrb(-/-) mice were markedly improved by introducing an Ednrb transgene under control of the dopamine β-hydroxylase promoter (Ednrb(-/-);DBH-Ednrb mice) on P19. Neither defects of melanocytes nor hypopigmentation in the SV and skin in Ednrb(-/-) mice was rescued in the Ednrb(-/-);DBH-Ednrb mice. Thus, the results of this study indicate a novel role of Ednrb expressed in SGNs distinct from that in melanocytes in the SV contributing partially to postnatal hearing development.
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