Korean J Med.
2003 Nov;65(5):549-557.
Regulatory mechanism of the sodium-iodide symporter by iodide in thyroid cells
- Affiliations
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- 1Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea. bycho@plaza.snu.ac.kr
- 2The Institute of Endocrinology, Nutrition and Metabolism, Seoul National University College of Medicine, Seoul, Korea.
- 3Seoul Municipal Boramae Hospital, Seoul, Korea.
- 4Clinical Research Institute Hormone Research Center and Laboratory for Eexperimental Animal Research, Seoul National University Hospital, Seoul Korea.
- 5Genomic Research Center for Diabetes and Endocrine Disease, Seoul Korea.
- 6Department of Internal Medicine, Ulsan University College of Medicine, Ulsan, Korea.
Abstract
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BACKGROUN: The sodium-iodide symporter (NIS) is a key plasma membrane glycoprotein that mediates active iodide transport in the thyroid gland. Whereas relatively little is known about the mechanisms by which iodide regulates NIS activity, post-transcriptional events have been suggested to play a role.
METHODS
We have attempted to determine the mechanism responsible for the regulation of NIS by determining NIS mRNA and NIS protein levels accompany with measuring NIS activities in FRTL-5 thyroid cells or Sprague-Dawley rats.
RESULTS
TSH increased the iodide uptake capacities and the expression of NIS mRNA by time- and concentration-dependent manner. This finding was also true in Sprague-Dawley rats whose serum TSH were elevated by prolonged methimazole administration; the expression of NIS protein was increased in TSH-elevated rats. On the other hands, iodide suppressed the NIS activity by concentration-dependent manner till 1 mM of NaI. But, the amounts of NIS mRNA were not changed, although those were transiently decreased at 24 hours after iodide treatment at the higher concentration of NaI, 10 mM or over. The amounts of NIS protein, which were analyzed by immunohistochemstry, were decreased till first 24 hours, but those were re-increased, the amounts at 48 hours after iodide treatment returned to more than 50% of basal levels.
CONCLUSION
TSH induced the expression of NIS, while iodide inhibited the NIS activities. Our finding suggested that the excessive iodide regulates the NIS activity, at least in part, through post-translational as well as transcriptional and translational mechanisms.
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