Gene Expression And Regulation Of Sodium Iodide Symporter In Thyroid Gland

Objective To investigate the gene expression of sodium iodide symporter (MS) in thyroid gland and the influence of hormones, iodine and retinoic acid on NIS mRNA expression in thyroid cells, and study the significance of these factors in the pathogenesis and treatment of thyroid disease.Methods The level of MS gene expression was evaluated by semi-quantitative reverse transcription polymerase chain reaction(RT-PCR). Total RNA was extracted from thyroid tissues. The cDNA was prepared by reverse transcription and amplified for NIS by PCR. Thyroid cells were cultured and stimulated with thyroid stimulating hormone(TSH), dexamethasone(Dex), estrogen(E2), testosterone(Te), retinoic acid(RA) and iodine. NIS antibody in the sera from GD and HT patients was detected by enzyme-linked immunosorbent assay (ELISA).Results (1) MS mRNA was detected in normal thyroid tissues, the level of MS mRNA was highly increased in GD thyroid tissues, while in HT thyroid tissues its level was decreased and even undetectable in some samples. MS mRNA could not be detected in thyroid carcinoma tissues. (2) The expression of MS gene was increased by TSH and all-trans retinoic acid, while MS mRNA levels were decreased by testosterone, dexamethasone, estrogen and iodine. (3) MS antibody in GD sera was significantly higher than healthy subjects and HT patients.Conclusions (1) The gene expression of MS is increased in GD thyroid tissues and MS antibody is significantly higher in GD patients,suggesting that NIS plays an important role in the pathogenesis of Graves' disease. (2) The NIS mRNA does not detected in thyroid carcinoma tissues, indicating that these tissues are unable to uptake radioiodide for ablation therapy. TSH and retinoic acid can up-regulate NIS mRNA level in thyrocytes and make thyroid carcinoma cells treatable by radioactive iodine. (3) The level of NIS mRNA can be decreased by some thyroid regulating factors such as testosterone, dexamethasone and so on, which may participate in the pathogenesis of thyroid disease.