Thyroxine treatments do not correct inner ear defects in tmprss1 mutant mice
- Author(s)
- Hanifa, S; Scott, HS; Crewther, P; Guipponi, M; Tan, J;
- Details
- Publication Year 2010-09-15,Volume 21,Issue #13,Page 897-901
- Journal Title
- NEUROREPORT
- Publication Type
- Journal Article
- Abstract
- Complete deficiency of a member of the type II transmembrane serine protease family, tmprss1 (also known as hepsin), is associated with severe to profound hearing loss in mice and a gross enlargement of the tectorial membrane in the cochlea. Levels of thyroxine in these mice have been shown to be significantly lower when compared with wild-type controls. As thyroxine is critical for inner ear development, we delivered thyroxine to these mice during the prenatal or postnatal stage of development. Both the treatments could not ameliorate hearing loss or correct deformities in the tectorial membrane of these mutant mice, suggesting that a deficiency in tmprss1 affects thyroxine responsiveness in the inner ear in vivo. NeuroReport 21: 897-901 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
- Publisher
- LIPPINCOTT WILLIAMS & WILKINS
- Keywords
- TRANSMEMBRANE SERINE-PROTEASE; AUTOSOMAL RECESSIVE DEAFNESS; HEARING-LOSS; THYROID-HORMONE; BETA GENE; EXPRESSION; RESISTANCE; DEFICIENT; MUTATIONS; FAMILIES
- Publisher's Version
- https://doi.org/10.1097/WNR.0b013e32833dbd2d
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2010-09-15 12:00:00