ArticleMolecular and cellular endocrinology2015
The timecourse of apoptotic cell death during postnatal remodeling of the mouse cochlea and its premature onset by triiodothyronine (T3).
Article in Molecular and cellular endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- 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
- Cellular expression domains of type 3 deiodinase in the meninges, choroid plexus, tanycytes and barrier tissues of the brain.Frontiers in endocrinology · 2026Article
- ZBTB20 is essential for cochlear maturation and hearing in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Thyroid hormone as a temporal switch in mouse development.European thyroid journal · 2023Review
- The Dual Roles of Triiodothyronine in Regulating the Morphology of Hair Cells and Supporting Cells during Critical Periods of Mouse Cochlear Development.International journal of molecular sciences · 2023Article
- Article
- Thyroxine Regulates the Opening of the Organ of Corti through Affecting P-Cadherin and Acetylated Microtubule.International journal of molecular sciences · 2022Article
- Kölliker's organ-supporting cells and cochlear auditory development.Frontiers in molecular neuroscience · 2022Review
- Cochlear Development; New Tools and Approaches.Frontiers in cell and developmental biology · 2022Review
- Cochlear Fibrocyte and Osteoblast Lineages Expressing Type 2 Deiodinase Identified with a Dio2CreERt2 Allele.Endocrinology · 2021Article
- Lineage-tracing and translatomic analysis of damage-inducible mitotic cochlear progenitors identifies candidate genes regulating regeneration.PLoS biology · 2021Article
- Thyroid Hormone Deiodinases: Dynamic Switches in Developmental Transitions.Endocrinology · 2021Review
- Single-Cell RNA Sequencing Analysis Reveals Greater Epithelial Ridge Cells Degeneration During Postnatal Development of Cochlea in Rats.Frontiers in cell and developmental biology · 2021Article
- Gpr125 Marks Distinct Cochlear Cell Types and Is Dispensable for Cochlear Development and Hearing.Frontiers in cell and developmental biology · 2021Article
- Transcription Factor Reprogramming in the Inner Ear: Turning on Cell Fate Switches to Regenerate Sensory Hair Cells.Frontiers in cellular neuroscience · 2021Article
- Programmed Cell Death Recruits Macrophages Into the Developing Mouse Cochlea.Frontiers in cell and developmental biology · 2021Article
- Autophagy precedes apoptosis during degeneration of the Kölliker's organ in the development of rat cochlea.European journal of histochemistry : EJH · 2019Article
- Deafness and loss of cochlear hair cells in the absence of thyroid hormone transporters Slc16a2 (Mct8) and Slc16a10 (Mct10).Scientific reports · 2018Article
- Article
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4 authors.
Funding
Abstract
Apoptosis underlies various forms of tissue remodeling during development. Prior to the onset of hearing, thyroid hormone (T3) promotes cochlear remodeling, which involves regression of the greater epithelial ridge (GER), a transient structure of columnar cells adjacent to the mechanosensory hair cells. We investigated the timecourse of apoptosis in the GER and the influence of ectopic T3 on apoptosis. In saline-treated mice, activated caspase 3-positive cells were detected in the GER between postnatal days 7 and 13 and appeared progressively along the cochlear duct from base to apex over developmental time. T3 given on P0 and P1 advanced the overall program of apoptosis and remodeling by ~4 days. Thyroid hormone receptor β was required for these actions, suggesting a receptor-mediated process of initiation of apoptosis. Finally, T3 given only at P0 or P1 resulted in deafness in adult mice, thus revealing a transient period of susceptibility to long-term damage in the neonatal auditory system.
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