ECE2016 Oral Communications Receptors & Signalling (5 abstracts)
Expression levels of thyroglobulin processing proteases are reduced upon trace amine-associated receptor 1 deficiency in mice
Joanna Szumska 1 , Zaina Batool 1 , Maria Qatato 1 , Emily Melisa Ullrich Gavilanes 1 , Vladislav Skripnik 1 , Nita Shillova 1 , David K. Grandy 2 & Klaudia Brix 1
1Jacobs University, Bremen, Germany; 2Oregon Health & Science University, Portland, Oregon, USA.
The function of the thyroid gland is to maintain thyroid hormone (TH) levels in the blood circulation. Thyroid epithelial cells liberate TH from the precursor molecule thyroglobulin (Tg) by the combined proteolytic action of the cathepsin B, K, L, and S. Cathepsin L-deficiency in mice results in impaired processing of Tg and remnants of dead cells in the follicle lumen. Recently, we have shown that Trace amine-associated receptor 1 (Taar1) is localized on the primary cilia of mouse thyrocytes. Interestingly, Taar1-deficient mice are characterized by remnants of dead cells in the follicle lumen; a phenotype shared with cathepsin L-deficient mice. Thus we investigated the possible link between expression and function of Taar1 and the activity of cathepsins B, K, L and S in vitro and in vivo. Pharmacological knock-down (Cathepsin L inhibitor III) of cathepsin L activity in FRT cells resulted in reduced immunoreactivity of Taar1 on their primary cilia. In mice (n=6) lacking Taar1, the expression in situ of cathepsin B, D and L was measured and cathepsin D and L expression levels were found to be reduced in 12 month old Taar1-deficient mice. We interpret these data to suggest that signalling mediated by Taar1 on the cilia of thyrocytes is critical for thyrocyte maturation and survival because it is involved in regulating the expression and activity of the cathepsins including cathepsin L that is critical to thyrocyte survival, TH processing and follicle maturation.
Supported by the Deutsche Forschungsgemeinschaft in the framework of SPP 1629/2, BR 1308/11-1, and 11-2.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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