ArticleAmerican journal of physiology. Renal physiology2009
Developmental delays consistent with cochlear hypothyroidism contribute to failure to develop hearing in mice lacking Slc26a4/pendrin expression.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 65 citations in OpenAlex.
- Substrate for Thyroid Hormone Synthesis: Biochemistry, Evolution, and Physiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- The Role of Thyroid Hormone Signaling in the Development and Pathophysiology of Hearing: From Molecular Mechanisms to Clinical Applications.International journal of molecular sciences · 2026Review
- AAV-mediated Gene Therapy for Hereditary Deafness: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- The role ofFrontiers in molecular neuroscience · 2024Review
- Cross-species applicability of an adverse outcome pathway network for thyroid hormone system disruption.Toxicological sciences : an official journal of the Society of Toxicology · 2023Review
- Three-dimensionally visualized ossification and mineralization process of the otic capsule in a postnatal developmental mouse.Laryngoscope investigative otolaryngology · 2023Article
- Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7.Communications biology · 2019Article
- How pH is regulated during amelogenesis in dental fluorosis.Experimental and therapeutic medicine · 2018Review
- Claudin expression during early postnatal development of the murine cochlea.BMC physiology · 2018Article
- Characterization of Wnt and Notch-Responsive Lgr5+ Hair Cell Progenitors in the Striolar Region of the Neonatal Mouse Utricle.Frontiers in molecular neuroscience · 2018Article
- Iodide Binding in Sodium-Coupled Cotransporters.Journal of chemical information and modeling · 2017Article
- Overexpression of Interleukin-4 in the Thyroid of Transgenic Mice Upregulates the Expression of Duox1 and the Anion Transporter Pendrin.Thyroid : official journal of the American Thyroid Association · 2016Article
- Genome-wide association study for acute otitis media in children identifies FNDC1 as disease contributing gene.Nature communications · 2016Article
- Atrophic thyroid follicles and inner ear defects reminiscent of cochlear hypothyroidism in Slc26a4-related deafness.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Article
- Article
- Slc26a7 chloride channel activity and localization in mouse Reissner's membrane epithelium.PloS one · 2014Article
- Differences in the pathogenicity of the p.H723R mutation of the common deafness-associated SLC26A4 gene in humans and mice.PloS one · 2014Article
- Article
- Mouse models for pendrin-associated loss of cochlear and vestibular function.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2013Review
- Endolymphatic Na⁺ and K⁺ concentrations during cochlear growth and enlargement in mice lacking Slc26a4/pendrin.PloS one · 2013Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations of SLC26A4 cause an enlarged vestibular aqueduct, nonsyndromic deafness, and deafness as part of Pendred syndrome. SLC26A4 encodes pendrin, an anion exchanger located in the cochlea, thyroid, and kidney. The goal of the present study was to determine whether developmental delays, possibly mediated by systemic or local hypothyroidism, contribute to the failure to develop hearing in mice lacking Slc26a4 (Slc26a4(-/-)). We evaluated thyroid function by voltage and pH measurements, by array-assisted gene expression analysis, and by determination of plasma thyroxine levels. Cochlear development was evaluated for signs of hypothyroidism by microscopy, in situ hybridization, and quantitative RT-PCR. No differences in plasma thyroxine levels were found in Slc26a4(-/-) and sex-matched Slc26a4(+/-) littermates between postnatal day 5 (P5) and P90. In adult Slc26a4(-/-) mice, the transepithelial potential and the pH of thyroid follicles were reduced. No differences in the expression of genes that participate in thyroid hormone synthesis or ion transport were observed at P15, when plasma thyroxine levels peaked. Scala media of the cochlea was 10-fold enlarged, bulging into and thereby displacing fibrocytes, which express Dio2 to generate a cochlear thyroid hormone peak at P7. Cochlear development, including tunnel opening, arrival of efferent innervation at outer hair cells, endochondral and intramembraneous ossification, and developmental changes in the expression of Dio2, Dio3, and Tectb were delayed by 1-4 days. These data suggest that pendrin functions as a HCO3- transporter in the thyroid, that Slc26a4(-/-) mice are systemically euthyroid, and that delays in cochlear development, possibly due to local hypothyroidism, lead to the failure to develop hearing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.