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Thyroxine treatments do not correct inner ear defects in tmprss1 mutant mice

Hanifa, Syazana
Crewther, Pauline
Tan, Justin
Published in Neuroreport. 2010, vol. 21, no. 13, p. 897-901
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.
Keywords AnimalsEar Diseases/congenital/*drug therapy/pathologyEar, Inner/*abnormalities/pathologyHearing/physiologyHearing TestsMiceMice, KnockoutMutation/physiologyReverse Transcriptase Polymerase Chain ReactionSerine Endopeptidases/*genetics/physiologyThyroxine/*therapeutic use
PMID: 20683358
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HANIFA, Syazana et al. Thyroxine treatments do not correct inner ear defects in tmprss1 mutant mice. In: Neuroreport, 2010, vol. 21, n° 13, p. 897-901. https://archive-ouverte.unige.ch/unige:20633

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Deposited on : 2012-05-22

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