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Acoustic trauma reduces SLC4A11 expression in the mouse cochlea
Author(s) -
Yamomoto Hiroshi,
Wilson Teresa,
Omelchenko Irina,
Zhang Yuan,
Nakashima Tsutomu,
Shi Xiaorui,
Nuttall Alfred L.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.694.7
Subject(s) - cochlea , inner ear , kidney , homeostasis , gene , hypoxia (environmental) , microbiology and biotechnology , gene expression , biology , chemistry , anatomy , endocrinology , genetics , organic chemistry , oxygen
Rationale The solute carrier 4A11 (SLC4A11) protein, a plasma membrane bound sodium‐borate co‐transporter, is expressed in many different organs including salivary glands, kidney, cornea and the inner ear where it functions to maintain ion homeostasis. Its functional importance is underscored by the causative role of SLC4A11 gene mutations in several inherited diseases, all of which are characterized by some form of sensorineural defect. Objective To compare SLC4A11 gene expression with other members of the SLC4 family in the inner ear, eye and kidney and to examine the affect of acoustic trauma on its expression in the cochlea. Methods and Results By quantitative real‐time PCR and immunoblot analysis, SLC4A11 transcript and protein levels in whole cochlea were markedly higher relative to eye and kidney, whereas SLC4A2 and SLC4A7 gene expression was quantitatively comparable among the three organs. Acoustic trauma resulted in a significant decrease in SLC4A11 transcript levels in the cochlear lateral wall. Further studies on cultured endothelial cells with chemical hypoxia mimetics revealed that down‐regulation of SLC4A11 can be mediated by hypoxia inducible factor. Conclusion Hypoxia, a major source of damage to cochlear tissues from acoustic trauma, may be the mechanism responsible for the reduced levels of SLC4A11. Supported by grants 5R01DC000105 (ALN), 1R01DC010844 (XS), and P30DC005983.