ArticleJournal of the Association for Research in Otolaryngology : JARO2008
Functional prestin transduction of immature outer hair cells from normal and prestin-null mice.
Article in Journal of the Association for Research in Otolaryngology : JARO, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Phosphorylation of MYL12 by Myosin Light Chain Kinase Regulates Cellular Shape Changes in Cochlear Hair Cells.Journal of the Association for Research in Otolaryngology : JARO · 2021Article
- Membrane prestin expression correlates with the magnitude of prestin-associated charge movement.Hearing research · 2016Article
- Activity-dependent regulation of prestin expression in mouse outer hair cells.Journal of neurophysiology · 2015Article
- Vibration of the organ of Corti within the cochlear apex in mice.Journal of neurophysiology · 2014Article
- A synthetic prestin reveals protein domains and molecular operation of outer hair cell piezoelectricity.The EMBO journal · 2011Article
- Deficient forward transduction and enhanced reverse transduction in the alpha tectorin C1509G human hearing loss mutation.Disease models & mechanismsArticle
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Authors and funding
7 authors.
Funding
Abstract
Prestin is a membrane protein in the outer hair cell (OHC) that has been shown to be essential for electromotility. OHCs from prestin-null mice do not express prestin, do not have a nonlinear capacitance (the electrical signature of electromotility), and are smaller in size than wild-type OHCs. We sought to determine whether prestin-null OHCs can be transduced to incorporate functional prestin protein in a normal fashion. A recombinant helper-dependent adenovirus expressing prestin and green fluorescent protein (HDAd-prestin-GFP) was created and tested in human embryonic kidney cells (HEK cells). Transduced HEK cells demonstrated membrane expression of prestin and nonlinear capacitance. HDAd-prestin-GFP was then applied to cochlear sensory epithelium explants harvested from wild-type and prestin-null mice at postnatal days 2-3, the age at which native prestin is just beginning to become functional in wild-type mice. At postnatal days 4-5, we investigated transduced OHCs for (1) their prestin expression pattern as revealed by immunofluorescence; (2) their cell surface area as measured by linear capacitance; and (3) their prestin function as indicated by nonlinear capacitance. HDAd-prestin-GFP efficiently transduced OHCs of both genotypes and prestin protein localized to the plasma membrane. Whole-cell voltage clamp studies revealed a nonlinear capacitance in transduced wild-type and prestin-null OHCs, but not in non-transduced cells of either genotype. Prestin transduction did not increase the linear capacitance (cell surface area) for either genotype. In peak nonlinear capacitance, voltage at peak nonlinear capacitance, charge density of the nonlinear capacitance, and shape of the voltage-capacitance curves, the transduced cells of the two genotypes resembled each other and previously reported data from adult wild-type mouse OHCs. Thus, prestin introduced into prestin-deficient OHCs segregates normally to the cell membrane and generates a normal nonlinear capacitance, indicative of normal prestin function.
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