ArticlePloS one2011
Epithelial cell stretching and luminal acidification lead to a retarded development of stria vascularis and deafness in mice lacking pendrin.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 68 citations in OpenAlex.
- A single-nucleus transcriptomic atlas of human inner ear development.Nature neuroscience · 2026Article
- Inhibitors of the ubiquitin‑proteasome system rescue cellular levels and ion transport function of pathogenic pendrin (SLC26A4) protein variants.International journal of molecular medicine · 2025Article
- Article
- Common genetic etiologies of sensorineural hearing loss in Koreans.Genomics & informatics · 2024Review
- SLC26A4-AP-2 mu2 interaction regulates SLC26A4 plasma membrane abundance in the endolymphatic sac.Science advances · 2024Article
- The role ofFrontiers in molecular neuroscience · 2024Review
- Single-cell RNA-sequencing of stria vascularis cells in the adult Slc26a4BMC medical genomics · 2023Article
- Molecular Features of SLC26A4 Common Variant p.L117F.Journal of clinical medicine · 2022Article
- Genetic architecture and phenotypic landscape of SLC26A4-related hearing loss.Human genetics · 2022Review
- Cochlear Pathomorphogenesis of Incomplete Partition Type II in Slc26a4-Null Mice.Journal of the Association for Research in Otolaryngology : JARO · 2021Article
- Development and evolution of the vestibular apparatuses of the inner ear.Journal of anatomy · 2021Review
- Genetic Determinants of Non-Syndromic Enlarged Vestibular Aqueduct: A Review.Audiology research · 2021Review
- Advances and challenges in adeno-associated viral inner-ear gene therapy for sensorineural hearing loss.Molecular therapy. Methods & clinical development · 2021Review
- Dissection of the Endolymphatic Sac from Mice.Journal of visualized experiments : JoVE · 2021Article
- Toward the Pathogenicity of theInternational journal of molecular sciences · 2021Article
- [The value of genetic diagnosis of deafness in evaluating the prognosis of cochlear implantation].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2021Article
- Adeno-associated virus gene replacement for recessive inner ear dysfunction: Progress and challenges.Hearing research · 2020Review
- Prenatal electroporation-mediated gene transfer restores Slc26a4 knock-out mouse hearing and vestibular function.Scientific reports · 2019Article
- Gene therapy for hereditary hearing loss by SLC26A4 mutations in mice reveals distinct functional roles of pendrin in normal hearing.Theranostics · 2019Article
- Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Loss-of-function mutations of SLC26A4/pendrin are among the most prevalent causes of deafness. Deafness and vestibular dysfunction in the corresponding mouse model, Slc26a4(-/-), are associated with an enlargement and acidification of the membranous labyrinth. Here we relate the onset of expression of the HCO(3) (-) transporter pendrin to the luminal pH and to enlargement-associated epithelial cell stretching. We determined expression with immunocytochemistry, cell stretching by digital morphometry and pH with double-barreled ion-selective electrodes. Pendrin was first expressed in the endolymphatic sac at embryonic day (E) 11.5, in the cochlear hook-region at E13.5, in the utricle and saccule at E14.5, in ampullae at E16.5, and in the upper turn of the cochlea at E17.5. Epithelial cell stretching in Slc26a4(-/-) mice began at E14.5. pH changes occurred first in the cochlea at E15.5 and in the endolymphatic sac at E17.5. At postnatal day 2, stria vascularis, outer sulcus and Reissner's membrane epithelial cells, and utricular and saccular transitional cells were stretched, whereas sensory cells in the cochlea, utricle and saccule did not differ between Slc26a4(+/-) and Slc26a4(-/-) mice. Structural development of stria vascularis, including vascularization, was retarded in Slc26a4(-/-) mice. In conclusion, the data demonstrate that the enlargement and stretching of non-sensory epithelial cells precedes luminal acidification in the cochlea and the endolymphatic sac. Stretching and luminal acidification may alter cell-to-cell communication and lead to the observed retarded development of stria vascularis, which may be an important step on the path to deafness in Slc26a4(-/-) mice, and possibly in humans, lacking functional pendrin expression.
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