Effect of thyroid statuses on sodium/iodide symporter (NIS) gene expression in the extrathyroidal tissues in mice

Abstract

BackgroundIodide that is essential for thyroid hormone synthesis is actively transported into the thyroid follicular cells via sodium/iodide symporter (NIS) protein in vertebrates. It is well known that NIS expression in thyroid is regulated by the thyroid statuses mainly through thyroid stimulating hormone (TSH). Although NIS mRNA expressions in extrathyroidal tissues have been qualitatively reported, their regulation by thyroid statuses has not been well clarified.MethodsMale ICR mice aged four weeks were assigned into three groups (control, hypothyroid, and hyperthyroid). Hypothyroid group of mice were treated with 0.02% methimazole in drinking water and hyperthyroid group of mice received intraperitoneal injection (4 μg L-T4 twice a week) for four weeks. NIS mRNA expression levels in the tissues were evaluated using Northern blot hybridization and quantitative real-time RTPCR (qPCR). Additionally, end-point RTPCR for the thyroid follicular cell-characteristic genes (TSH receptor, TSHR; thyroid transcription factor-1, TTF1; and paired box gene 8, Pax8) was carried out.ResultsBy Northern blot analysis, NIS mRNA was detected in thyroid and stomach. In addition to these organs, qPCR revealed the expression also in the submandibular gland, colon, testis, and lung. Expression of NIS mRNA in thyroid was significantly increased in hypothyroid and decreased in hyperthyroid group. Trends of NIS mRNA expression in extrathyroidal tissues were not in line with that in the thyroid gland in different thyroid statuses. Only in lung, NIS mRNA was regulated by thyroid statuses but in opposite way compared to the manner in the thyroid gland. There were no extrathyroidal tissues that expressed all three characteristic genes of thyroid follicular cells.ConclusionsNIS mRNA expression in the thyroid gland was up-regulated in hypothyroid mice and was down-regulated in hyperthyroid mice, suggesting that NIS mRNA in the thyroid gland is regulated by thyroid statuses. In contrast, NIS mRNA expression in extrathyroidal tissues was not altered by thyroid statuses although it was widely expressed. Lack of responsiveness of NIS mRNA expressions in extrathyroidal tissues reemphasizes additional functions of NIS protein in extrathyroidal tissues other than iodide trapping.

Hypothyroxinemia Induced by Mild Iodine Deficiency Deregulats Thyroid Proteins during Gestation and Lactation in Dams

“…NIS plays key roles in transporting iodide to the gland [18]. Compared with the control group, the significant up-regulations of thyroidal NIS were observed in rats exposed to the mild ID and severe ID groups on GD19 and PN21 ( p < 0.05, Figure 5(B)).…”

“…TTF1 and PAX8 have been shown to regulate expression of thyroid-specific genes, such as Na + /I − symporter (NIS) [16,17]. As the thyroid iodide transporter, NIS plays a key role in iodide concentration that is an essential step in thyroid hormone (TH) synthesis [18]. Many kinds of thyroid disorders and ID are implicated in the alterations of the NIS gene [19,20].…”

Does iodine gas released from seaweed contribute to dietary iodine intake?

“…The earlier work of Morgan et al (1968) suggested deposition of particle-associated I 2 in the nasopharyngeal tract as the major source of ingestion. As the sodium iodide transporter NIS has only rarely been demonstrated in lung tissue (Spitzweg et al 1998;Harun-Or-Rashid et al 2010), deposition may indeed be the most efficient pathway. However, more recent work by Harvey et al (2006;Harvey 2009) documented differences in gas uptake from that occurring as a result of particle deposition.…”

Thyroid hormone status affects expression of daily torpor and gene transcription in Djungarian hamsters (Phodopus sungorus)

“…Doses adapted from studies in mice and rats were tested in a pilot-study (Hamidi et al, 2010;Harun-Or-Rashid et al, 2010). T3 and T4 were dissolved in 0.025% sodium hydroxide (0.1N) and tap water.…”