Ajjan R A, Kamaruddin N A, Crisp M, Watson P F, Ludgate M, Weetman A P
Department of Medicine, University of Sheffield, UK.
Clin Endocrinol (Oxf). 1998 Oct;49(4):517-23. doi: 10.1046/j.1365-2265.1998.00570.x.
Iodide uptake by the thyroid gland is mediated by the sodium iodide symporter (NIS). In the present report, we have analysed the factors that modulate human NIS mRNA expression and iodide uptake in primary thyroid follicular cell (TFC) cultures. In addition, NIS mRNA tissue distribution was investigated.
Primary thyroid follicular cell cultures were treated with human recombinant TSH with or without cytokines for 72 h. Subsequently, NIS gene expression and iodide uptake were analysed using reverse transcription-polymerase chain reaction (RT-PCR) and 125I uptake, respectively. Human tissue samples were investigated for NIS gene expression using both RT-PCR and Northern blotting.
Human TSH increased both NIS gene expression and iodide uptake in TFC cultures in a dose-dependent manner. Using concentrations of 0.1 U/l of hTSH, a minor increase in NIS gene expression was detected without a detectable increase in iodide uptake. IL-1 alpha, TNF alpha and IFN gamma at concentrations of 10(5) U/l all inhibited TSH-induced NIS gene expression and iodide uptake. In these experiments, there was a good correlation between NIS mRNA expression and iodide uptake. Using RT-PCR higher levels of NIS mRNA were detected in Graves' disease (GD) compared to multi-nodular goitre tissue samples. Stomach and salivary gland tissue also expressed NIS mRNA, whereas low levels were found in the mammary gland and extraocular muscle tissue. No expression was detected in the ovary, oesophagus, colon, extraocular fat or skin. In contrast, Northern blot analysis failed to detect NIS in stomach, salivary gland, intestinal fat or non-toxic multi-nodular goitre tissue samples, although this was present in GD thyroid tissue.
TSH upregulates sodium iodide symporter gene expression and iodide uptake in primary thyroid follicular cell cultures, and this induction is modulated by cytokines. Variable levels of sodium iodide symporter mRNA are present in different tissue samples, with high expression evident in Graves' disease thyroid tissue.
甲状腺对碘化物的摄取由钠碘同向转运体（NIS）介导。在本报告中，我们分析了在原代甲状腺滤泡细胞（TFC）培养物中调节人NIS mRNA表达和碘化物摄取的因素。此外，还研究了NIS mRNA的组织分布。
原代甲状腺滤泡细胞培养物用重组人促甲状腺激素（TSH）处理，有或无细胞因子，处理72小时。随后，分别使用逆转录-聚合酶链反应（RT-PCR）和125I摄取分析NIS基因表达和碘化物摄取。使用RT-PCR和Northern印迹法研究人组织样本中的NIS基因表达。
重组人TSH以剂量依赖性方式增加TFC培养物中的NIS基因表达和碘化物摄取。使用0.1 U/l的hTSH浓度时，检测到NIS基因表达有轻微增加，但碘化物摄取没有可检测到的增加。浓度为10(5) U/l的白细胞介素-1α（IL-1α）、肿瘤坏死因子-α（TNFα）和干扰素-γ（IFNγ）均抑制TSH诱导的NIS基因表达和碘化物摄取。在这些实验中，NIS mRNA表达与碘化物摄取之间存在良好的相关性。使用RT-PCR检测到，与多结节性甲状腺肿组织样本相比，格雷夫斯病（GD）中NIS mRNA水平更高。胃和唾液腺组织也表达NIS mRNA，而在乳腺和眼外肌组织中水平较低。在卵巢、食管、结肠、眼外脂肪或皮肤中未检测到表达。相比之下，Northern印迹分析未能在胃、唾液腺、肠脂肪或非毒性多结节性甲状腺肿组织样本中检测到NIS，尽管在GD甲状腺组织中存在。
TSH上调原代甲状腺滤泡细胞培养物中钠碘同向转运体基因表达和碘化物摄取，且这种诱导受细胞因子调节。不同组织样本中存在不同水平的钠碘同向转运体mRNA, 在GD甲状腺组织中表达明显升高。
