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Divergent roles for thyroid hormone receptor beta isoforms in the endocrine axis and auditory system.

http://www.ncbi.nlm.nih.gov/pubmed/10430610

Thyroid hormone receptors (TRs) modulate various physiological functions in many organ systems. The TR alpha and TR beta isoforms are products of 2 distinct genes, and the beta 1 and beta 2 isoforms are splice variants of the same gene. Whereas TR alpha 1 and TR beta 1 are widely expressed, expression of the TR beta 2 isoform is mainly limited to the pituitary, triiodothyronine-responsive TRH neurons, the developing inner ear, and the retina. Mice with targeted disruption of the entire TR beta locus (TR beta-null) exhibit elevated thyroid hormone levels as a result of abnormal central regulation of thyrotropin, and also develop profound hearing loss. To clarify the contribution of the TR beta 2 isoform to the function of the endocrine and auditory systems in vivo, we have generated mice with targeted disruption of the TR beta 2 isoform. TR beta 2-null mice have preserved expression of the TR alpha and TR beta 1 isoforms. They develop a similar degree of central resistance to thyroid hormone as TR beta-null mice, indicating the important role of TR beta 2 in the regulation of the hypothalamic-pituitary-thyroid axis. Growth hormone gene expression is marginally reduced. In contrast, TR beta 2-null mice exhibit no evidence of hearing impairment, indicating that TR beta 1 and TR beta 2 subserve divergent roles in the regulation of auditory function.

Pubmed ID: 10430610 RIS Download

Mesh terms: Animals | Auditory Pathways | Crosses, Genetic | Evoked Potentials, Auditory, Brain Stem | Gene Expression Regulation | Growth Hormone | Ligands | Mice | Mice, Inbred C57BL | Mice, Knockout | Protein Isoforms | Receptors, Thyroid Hormone | Thyrotropin | Thyroxine | Triiodothyronine

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Associated grants

  • Agency: NIDDK NIH HHS, Id: DK-02485
  • Agency: NIDDK NIH HHS, Id: DK-49126
  • Agency: NIDDK NIH HHS, Id: DK-50564

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