Referenced in: none

Automatically associated channels: ClC4 , ClC5

Title: ClC-5 does not affect megalin expression and function in the thyroid.

Authors: Tanja Maritzen, Simonetta Lisi, Roberta Botta, Aldo Pinchera, Giovanni Fanelli, Paolo Viacava, Claudio Marcocci, Michele Marinò

Journal, date & volume: Thyroid, 2006 Aug , 16, 725-30

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/16910872

Abstract
Megalin is an endocytic receptor responsible for thyroglobulin (Tg) transcytosis, a process that favors hormone release. Accordingly, megalin KO mice have primary hypothyroidism. In the kidney, megalin expression is reduced when the gene encoding the chloride transporter ClC-5 is mutated. We investigated whether megalin expression and function in the thyroid are affected by ClC-5 using a ClC-5 KO mouse model. By Western blotting, ClC-5 was found in thyroid tissue extracts of WT, but not of ClC-5 KO mice. In addition, ClC-5 was found to be expressed by cultured thyroid cells (FRTL-5). The thyroid size, weight, and histology were similar in ClC- 5 KO and WT mice, as were the amounts of megalin in thyroid extracts. Accordingly, serum Tg, a measure of megalin-mediated transcytosis, was similar in WT and ClC-5 KO mice, suggesting that megalin function was unaffected. Thus, unlike in megalin KO mice, in ClC-5 KO mice thyroid function was unchanged, as indicated by the normal serum FT4 and TSH. We concluded that in the thyroid, unlike in the kidney, ClC-5 does not affect megalin expression and function, suggesting that megalin is differentially regulated in these two organs.