Chonnam Med J.  2000 Sep;36(3):297-306.

Effect of Lithium on Na+/I- Symporter Gene Expression in Rat Thyroid FRTL-5 Cells

Affiliations
  • 1Department of Internal Medicine, Chonnam National University Medical School.

Abstract

Lithium has been reported to alter thyroid function and cause goiter in some patients. To explain the mechanism of lithium action on thyroid iodide (I-) uptake at the molecular level, we studied, using functioning rat thyroid FRTL-5 cells, the effect of lithium on gene expression of Na+/I- symporter (NIS) by which I- is cotransported with Na+ into the thyroid cells. TSH-induced I- accumulation was suppressed by lithium at the concentration of 0.5 mM or higher in FRTL-5 cells. In contrast, lithium increased I- accumulation by decreasing I- release in CHO cells stably expressing a rat NIS cDNA. These results suggest that lithium could decrease NIS gene expression in FRTL-5 cells. Indeed, the TSH-induced increases in both NIS mRNA and NIS protein levels were suppressed by lithium treatment of FRTL-5 cells. Lithium also inhibited forskolin- and (Bu) 2cAMP-stimulated NIS mRNA levels as well as I- uptake by FRTL-5 cells; however, even 10 mM lithium did not affect TSH-induced cAMP production. In sum, suppression of I- transport activity by lithium in thyrocytes is partly due to a decrease in NIS gene expression, which is mediated at a step after cAMP production.

Keyword

Lithium; NIS; FRTL-5

MeSH Terms

Animals
CHO Cells
Cricetinae
DNA, Complementary
Gene Expression*
Goiter
Humans
Ion Transport*
Lithium*
Rats*
RNA, Messenger
Thyroid Gland*
DNA, Complementary
Lithium
RNA, Messenger
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