| First Author | Ng L | Year | 2015 |
| Journal | Endocrinology | Volume | 156 |
| Issue | 10 | Pages | 3853-65 |
| PubMed ID | 26241124 | Mgi Jnum | J:227423 |
| Mgi Id | MGI:5700451 | Doi | 10.1210/en.2015-1468 |
| Citation | Ng L, et al. (2015) Age-Related Hearing Loss and Degeneration of Cochlear Hair Cells in Mice Lacking Thyroid Hormone Receptor beta1. Endocrinology 156(10):3853-65 |
| abstractText | A key function of the thyroid hormone receptor beta (Thrb) gene is in the development of auditory function. However, the roles of the 2 receptor isoforms, TRbeta1 and TRbeta2, expressed by the Thrb gene are unclear, and it is unknown whether these isoforms promote the maintenance as well as development of hearing. We investigated the function of TRbeta1 in mice with a Thrb(b1) reporter allele that expresses beta-galactosidase instead of TRbeta1. In the immature cochlea, beta-galactosidase was detected in the greater epithelial ridge, sensory hair cells, spiral ligament, and spiral ganglion and in adulthood, at low levels in the hair cells, support cells and root cells of the outer sulcus. Although deletion of all TRbeta isoforms causes severe, early-onset deafness, deletion of TRbeta1 or TRbeta2 individually caused no obvious hearing loss in juvenile mice. However, over subsequent months, TRbeta1 deficiency resulted in progressive loss of hearing and loss of hair cells. TRbeta1-deficient mice had minimal changes in serum thyroid hormone and thyrotropin levels, indicating that hormonal imbalances were unlikely to cause hearing loss. The results suggest mutually shared roles for TRbeta1 and TRbeta2 in cochlear development and an unexpected requirement for TRbeta1 in the maintenance of hearing in adulthood. |
