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A “Tric” to tighten cell-cell junctions in the cochlea for hearing
Tomohito Higashi, … , Mikio Furuse, Karen B. Avraham
Tomohito Higashi, … , Mikio Furuse, Karen B. Avraham
Published August 27, 2013
Citation Information: J Clin Invest. 2013;123(9):3712-3715. https://doi.org/10.1172/JCI69651.
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Commentary

A “Tric” to tighten cell-cell junctions in the cochlea for hearing

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Abstract

Tricellulin is a tricellular tight junction–associated membrane protein that controls movement of solutes at these specialized cell intersections. Mutations in the gene encoding tricellulin, TRIC, lead to nonsyndromic deafness. In this issue of the JCI, Nayak et al. created a gene-targeted knockin mouse in order to mimic the pathology of a human TRIC mutation. Deafness appears to be caused either by an increase in the K+ ion concentration around the basolateral surfaces of the outer hair cells or, alternatively, by an increase in small molecules such as ATP around the hair bundle, leading to cellular dysfunction and degeneration. Furthermore, the mice have features suggestive of syndromic hearing loss, which may have implications for care and treatment of patients harboring TRIC mutations.

Authors

Tomohito Higashi, Danielle R. Lenz, Mikio Furuse, Karen B. Avraham

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Figure 1

The mammalian organ of Corti contains the sensory epithelium essential for hearing, including hair and supporting cells.

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The mammalian organ of Corti contains the sensory epithelium essential f...
The hair cells include both inner and outer hair cells, and the supporting cells include Hensen’s cells, Deiters’ cells, and pillar cells. A crucial parameter of the organ of Corti is the ionic composition of the perilymph and endolymph, held in balance by the epithelial sheet that contains TJs. A further demarcation of the TJs are the tTJs, which when impaired in Tric mutant mice are postulated to lead to endolymph leakage into the perilymph. This aberration would have dire consequences for hearing.
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