Intracellular iodinated compounds affect sodium iodide symporter expression through TSH-mediated signaling pathways

Huang, Huibin; Shi, Yue; Lin, Ling; Li, Xisheng; Li, Liangyi; Lin, Xiahong; Xu, Dongming

doi:10.3892/mmr.2010.384

Cited by 4 publications

(3 citation statements)

References 16 publications

(18 reference statements)

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“…One of the most important one is the transport of I − across the membrane of the thyroid follicular cells by NIS. In our study, NIC males displayed higher NIS protein expression, despite low TSH, which is a major stimulator of NIS expression 21 . As NIS activity was not measured, this can be considered a limitation of this study.…”

Section: Discussionsupporting

confidence: 46%

Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding

Miranda

Moura

Soares

et al. 2020

Sci Rep

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Maternal nicotine exposure causes several consequences in offspring phenotype, such as obesity and thyroid dysfunctions. Nicotine exposure can increase oxidative stress levels, which could lead to thyroid dysfunction. However, the mechanism by which nicotine exposure during breastfeeding leads to thyroid gland dysfunction remains elusive. We aimed to investigate the long-term effects of maternal nicotine exposure on redox homeostasis in thyroid gland, besides other essential steps for thyroid hormone synthesis in rats from both sexes. Lactating Wistar rats were implanted with osmotic minipumps releasing nicotine (NIC, 6 mg/kg/day) or saline (control) from postnatal day 2 to 16. Offspring were analyzed at 180-day-old. NIC males showed lower plasma TSH, T3 and T4 while NIC females had higher T3 and T4. In thyroid, NIC males had higher sodium-iodide symporter protein expression, whereas NIC females had higher thyroid-stimulating hormone receptor (TSHr) and thyroperoxidase (TPO) protein expression. TPO activity was lower in NIC males. Hydrogen peroxide generation was decreased in NIC males. Activities of superoxide dismutase, catalase and glutathione peroxidase were compromised in NIC animals from both sexes. 4-Hydroxynonenal was higher only in NIC females, while thiol was not affected in NIC animals from both sexes. NIC offspring also had altered expression of sex steroid receptors in thyroid gland. Both sexes showed similar thyroid morphology, with lower follicle and colloid size. Thyroid from female offspring exposed to nicotine during breastfeeding developed oxidative stress, while the male gland seemed to be protected from redox damage. Thyroid dysfunctions seem to be associated with redox imbalance in a sex-dependent manner.

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Section: Discussionsupporting

confidence: 46%

Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding

Miranda

Moura

Soares

et al. 2020

Sci Rep

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“…TSHr is activated by Gs protein, which can change adenylate cyclase activity and catalysis ATP converted into cyclization adenosine (cyclic adenylic acid, cAMP). Once the concentration of intracellular cAMP changed, the adjustment role of cAMP on cells is by activating the protein kinase A (protein kinase, PKA) system to realize the cascade reaction of cAMP that will eventually enhance gene expressions of thyroid specific transcription factors, such as TTf-1 gene expression and activity, thus improving the thyroid cell NIS mRNA and protein expression [ 28 , 29 , 30 ]. As a result, the thyroid iodine intake function is enhanced, possibly leading to decreased serum THs and urine iodine.…”

Section: Discussionmentioning

confidence: 99%

Effects of Long-Term In Vivo Exposure to Di-2-Ethylhexylphthalate on Thyroid Hormones and the TSH/TSHR Signaling Pathways in Wistar Rats

Dong

Zhao

et al. 2017

IJERPH

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Di-(2-ethylhexyl)phthalate (DEHP) was a widely used chemical with human toxicity. Recent in vivo and in vitro studies suggested that DEHP-exposure may be associated with altered serum thyroid hormones (THs) levels, but the underlying molecular mechanisms were largely unknown. To explore the possible molecular mechanisms, 128 Wistar rats were dosed with DEHP by gavage at 0, 150, 300, and 600 mg/kg/day for 3 months (M) and 6 M, respectively. After exposure, expression of genes and proteins in the thyroid, pituitary, and hypothalamus tissues of rats were analyzed by Q-PCR and western blot, while the sera and urine samples were assayed by radioimmunoassay and ELISA. Results showed that serum THs levels were suppressed by DEHP on the whole. DEHP treatment influenced the levels of rats’ thyrotropin releasing hormone receptor (TRHr), Deiodinases 1 (D1), thyroid stimulating hormone beta (TSHβ), sodium iodide symporter (NIS), thyroid stimulating hormone receptor (TSHr), thyroperoxidase (TPO), thyroid transcription factor 1 (TTF-1), and thyroglobulin (TG) mRNA/protein expression in the hypothalamus-pituitary-thyroid (HPT) axis and decreased urine iodine. Taken together, observed findings indicate that DEHP could reduce thyroid hormones via disturbing the HPT axis, and the activated TSH/TSHR pathway is required to regulate thyroid function via altering TRHr, TSHβ, NIS, TSHr, TPO, TTF-1 and TG mRNA/protein expression of the HPT axis.

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“…At the cellular level, iodine has been shown to inhibit multiple signaling pathways of thyroid cells, including CAMP and PIP2. Iodine not only reduces the expression of thyroid-specific proteins such as NIS but also has been shown to alter the TSH/TSHr signaling pathway [ 6 – 8 ]. At the follicular level, iodine in follicular lumen, namely, iodinated thyroglobulin (iodinated TG), is the main form of iodine reserve in the body.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of TSHR, TTF-1, and PAX8 in Nodular Goiter Is Associated with Iodine Deficiency in the Follicular Lumen

Huang

Chen

Liang

et al. 2016

International Journal of Endocrinology

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Objective. It has been testified that iodine regulates thyroid function by controlling thyroid-restricted genes expression and is closely related to diffuse goiter and thyroid dysfunction. However, the effects of follicular lumen iodine, the main form of iodine reserve in the body, on thyroid-restricted genes in nodular goiter are poorly understood. In this study, correlations between follicular lumen iodine and the expressions of thyroid stimulating hormone receptor (TSHR), its transcription factors TTF-1, and PAX8 in nodular goiter were investigated. Patients. In this study, 30 resection specimens clinically histopathologically confirmed to have nodular goiter and 30 normal thyroid specimens from adjacent tissues of nodular goiter are used. Measurement. Western blot immunohistochemistry was performed to assay TSHR, TTF-1, and PAX8 in thyrocytes of nodular goiter as well as in extranodular normal thyroid tissues. Meanwhile, follicular lumen iodine of both nodular goiter and extranodular normal thyroid tissues was detected as well. Results. The TSHR, TTF-1, and PAX8 in nodular goiter were significantly higher than those in the controls. The iodine content in nodular goiter was significantly lower than those in control tissues. Conclusion. Upregulation of TSHR, TTF-1, and PAX8 is associated with low follicular lumen iodine content in nodular goiter.

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Intracellular iodinated compounds affect sodium iodide symporter expression through TSH-mediated signaling pathways

Cited by 4 publications

References 16 publications

Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding

Thyroid redox imbalance in adult Wistar rats that were exposed to nicotine during breastfeeding

Effects of Long-Term In Vivo Exposure to Di-2-Ethylhexylphthalate on Thyroid Hormones and the TSH/TSHR Signaling Pathways in Wistar Rats

Upregulation of TSHR, TTF-1, and PAX8 in Nodular Goiter Is Associated with Iodine Deficiency in the Follicular Lumen

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