ArticleHistochemistry and cell biology2007
Thyroid hormone receptor alpha1 is a critical regulator for the expression of ion channels during final differentiation of outer hair cells.
Article in Histochemistry and cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 36 citations in OpenAlex.
- Age-related hearing loss pertaining to potassium ion channels in the cochlea and auditory pathway.Pflugers Archiv : European journal of physiology · 2021Review
- Recent advances in cochlear hair cell nanophysiology: subcellular compartmentalization of electrical signaling in compact sensory cells.Faculty reviews · 2020Review
- Gαi Proteins are Indispensable for Hearing.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Article
- Thyroid hormone is required for the pruning of afferent type II spiral ganglion neurons in the mouse cochlea.Neuroscience · 2016Article
- Unliganded thyroid hormone receptor α regulates developmental timing via gene repression in Xenopus tropicalis.Endocrinology · 2015Article
- Making sense with thyroid hormone--the role of T(3) in auditory development.Nature reviews. Endocrinology · 2013Review
- Reduced electromotility of outer hair cells associated with connexin-related forms of deafness: an in silico study of a cochlear network mechanism.Journal of the Association for Research in Otolaryngology : JARO · 2010Article
- Article
- Developmental delays consistent with cochlear hypothyroidism contribute to failure to develop hearing in mice lacking Slc26a4/pendrin expression.American journal of physiology. Renal physiology · 2009Article
- Deafness in TRbeta mutants is caused by malformation of the tectorial membrane.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- State-of-the-art technologies, current opinions and developments, and novel findings: news from the field of histochemistry and cell biology.Histochemistry and cell biology · 2008Review
- The influence of thyroid hormone deficiency on the development of cochlear nonlinearities.Journal of the Association for Research in Otolaryngology : JARO · 2008Article
- Functional prestin transduction of immature outer hair cells from normal and prestin-null mice.Journal of the Association for Research in Otolaryngology : JARO · 2008Article
- Mutations of ESRRB encoding estrogen-related receptor beta cause autosomal-recessive nonsyndromic hearing impairment DFNB35.American journal of human genetics · 2008Article
- Recent progress in histochemistry.Histochemistry and cell biology · 2007Review
- [Therapeutic use of stem cells].HNO · 2007Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cochlear outer hair cells (OHCs) terminally differentiate prior to the onset of hearing. During this time period, thyroid hormone (TH) dramatically influences inner ear development. It has been shown recently that TH enhances the expression of the motor protein prestin via liganded TH receptor beta (TRbeta) while in contrast the expression of the potassium channel KCNQ4 is repressed by unliganded TRalpha1. These different mechanisms of TH regulation by TRalpha1 or TRbeta prompted us to analyse other ion channels that are required for the final differentiation of OHCs. We analysed the onset of expression of the Ca(2+) channel Ca(V)1.3, and the K(+) channels SK2 and BK and correlated the results with the regulation via TRalpha1 or TRbeta. The data support the hypothesis that proteins expressed in rodents prior to or briefly after birth like Ca(V)1.3 and prestin are either independent of TH (e.g. Ca(V)1.3) or enhanced through TRbeta (e.g. prestin). In contrast, proteins expressed in rodents later than P6 like KCNQ4 ( approximately P6), SK2 ( approximately P9) and BK ( approximately P11) are repressed through TRalpha1. We hypothesise that the precise regulation of expression of the latter genes requires a critical local TH level to overcome the TRalpha1 repression.
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