Sodium iodide symporter gene expression in thyroid of mice with different iodine intakes / 中华内分泌代谢杂志

ABSTRACT

Objective To investigate the sodium iodide symporter (NIS) gene expression during different iodine intakes and its function in thyroid autoregulation. Methods BabL/c mice were randomly divided into five groups according to their different iodine intake levels : low iodine (LI), normal iodine (NI), five-fold iodine (5HI) ,ten-fold iodine (10 HI) and fifty-fold iodine (50 HI). After three months and six months administration, they were sacrificed and thyroids were excised. The mRNA and protein expression level were determined by real time quantitative PCR and immunohistochemistry respectively. Iodine content in thyroid tissue was measured with spectrophotometry and thyroid hormone level was measured with radioimmunoassay. Results Compared with NI group, NIS mRNA and protein expression was greatly increased in LI groups. Immunohistochemistry analysis indicated that NIS was mostly located at the basolateral membrane of thyrocyte,suggesting the improved activity in transporting iodine. But when faced with long-term and severe iodine deficiency, the iodine content in thyroid was finally decreased ,and hormone level lowered. On the other hand, in HI groups NIS mRNA and protein expression was greatly down-regulated. There was a tendency of decreasing NIS gene expression level with increasing doses of iodine intakes. In addition, NIS protein was found mainly in intracellular vesicles, rather than at the cell membrane,suggesting the loss of its activity. The iodine content in thyroid tissue was only slightly increased and was not consistent with the iodine intake levels. Conclusion These findings indicate that NIS may be. regulated at transcription, translation and post-translation levels. This phenomenon constitutes a highly specialized intrinsic autoregulatory system that protects thyroid from high doses of iodine, but at the same time ensures adequate iodine uptake for hormone biosynthesis. NIS plays a critical role in thyroid autoregulation mechanism.