Different expression of sodium-iodide importer (NIS) between lactating breast and thyroid tissues may be due to structural difference of thyroid-stimulating hormone receptor (TSHR).

Abstract

Thyroid-stimulating hormone (TSH) binds TSH receptor (TSHR) on thyroid cell membranes, which will lead activation of cyclic adenosine 3',5'-monophosphate/protein kinase A signaling pathway. Through this pathway, TSHR regulates the expression of sodium-iodide symporter (NIS) to complete iodine intake. In recent studies, it is found that TSHR is widely expressed in a variety of extra-thyroidal tissues. TSHR expressions as well as distribution in normal mammary gland tissues have not been reported. The physiological mechanism of the TSHR in the extra-thyroidal tissues has also been controversial. In this study, immunohistochemistry and immunofluorescence were used to characterize the expression distribution of TSHR protein in lactating breast. DNA sequence of TSHR cDNA from mice lactating breast was determined and then compared with TSHR cDNA from mice thyroidal tissue. A 173 amino acid (AA) fragment deletion was found in the extra-cellular domain of lactating breast TSHR. The expression levels of NIS mRNA were compared between two tissues, and the level of NIS mRNA in lactating breasts was lower than the one in thyroidal tissues. The lower expression of NIS in lactating breast may be due to the 173 AA deletion in the TSHR resulting the lower binding of TSH to the TSHR. For the first time, this finding may explain the reason of the lower NIS expression in lactating breast.