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碘化物治疗通过转录机制急性增加大鼠甲状腺和 PCCl3 甲状腺细胞系中的 pendrin (SLC26A4) mRNA 表达。

Iodide treatment acutely increases pendrin (SLC26A4) mRNA expression in the rat thyroid and the PCCl3 thyroid cell line by transcriptional mechanisms.

机构信息

Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, 05508-000 São Paulo, SP, Brazil.

出版信息

Mol Cell Endocrinol. 2012 Mar 5;350(1):118-24. doi: 10.1016/j.mce.2011.12.002. Epub 2011 Dec 9.

DOI:10.1016/j.mce.2011.12.002
PMID:22178794
Abstract

Iodine is a critical element involved in thyroid hormone synthesis. Its efflux into the follicular lumen is thought to occur, in part, through pendrin at the apical membrane of thyrocytes. This study attempted to investigate whether iodide administration affects SLC26A4 mRNA expression in rat thyroid and in PCCl3 cells. Rats and cells were treated or not with NaI from 30 min up to 48 h. One group was concomitantly treated with sodium perchlorate. SLC26A4 mRNA expression was also investigated in PCCl3 cells treated with actinomycin D prior to NaI treatment. Iodide administration significantly increased SLC26A4 mRNA content in both models. The simultaneous administration of NaI and perchlorate, as well as the treatment of PCCl3 cells with actinomycin D prevented this effect, indicating that intracellular iodide is essential for this event, which appears to be triggered by transcriptional mechanisms. These data show that intracellular iodide rapidly upregulates SLC26A4 mRNA expression.

摘要

碘是甲状腺激素合成中不可或缺的元素。人们认为,碘从甲状腺滤泡腔中的外流部分是通过甲状腺细胞顶膜上的 pendrin 发生的。本研究试图探讨碘化物给药是否会影响大鼠甲状腺和 PCCl3 细胞中 SLC26A4 mRNA 的表达。用 NaI 处理大鼠和细胞 30 分钟至 48 小时。一组同时用高氯酸钠处理。在给予 NaI 之前,还在 PCCl3 细胞中用放线菌 D 处理以研究 SLC26A4 mRNA 的表达。碘化物给药显著增加了两种模型中 SLC26A4 mRNA 的含量。同时给予 NaI 和高氯酸钠,以及用放线菌 D 处理 PCCl3 细胞均可阻止这种作用,表明细胞内碘是该事件所必需的,该事件似乎是由转录机制触发的。这些数据表明,细胞内碘可快速上调 SLC26A4 mRNA 的表达。

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1
Iodide treatment acutely increases pendrin (SLC26A4) mRNA expression in the rat thyroid and the PCCl3 thyroid cell line by transcriptional mechanisms.碘化物治疗通过转录机制急性增加大鼠甲状腺和 PCCl3 甲状腺细胞系中的 pendrin (SLC26A4) mRNA 表达。
Mol Cell Endocrinol. 2012 Mar 5;350(1):118-24. doi: 10.1016/j.mce.2011.12.002. Epub 2011 Dec 9.
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New insights about the posttranscriptional mechanisms triggered by iodide excess on sodium/iodide symporter (NIS) expression in PCCl3 cells.碘过量触发 PCCl3 细胞钠/碘同向转运体(NIS)表达的转录后机制的新见解。
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Posttranscriptional regulation of sodium-iodide symporter mRNA expression in the rat thyroid gland by acute iodide administration.急性碘处理对大鼠甲状腺钠碘同向转运体 mRNA 表达的转录后调控。
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Differential gene expression analysis of iodide-treated rat thyroid follicular cell line PCCl3.碘处理的大鼠甲状腺滤泡细胞系PCCl3的差异基因表达分析
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Underlying Mechanisms of Pituitary-Thyroid Axis Function Disruption by Chronic Iodine Excess in Rats.慢性碘过量致大鼠垂体-甲状腺轴功能紊乱的潜在机制
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PKC-epsilon-dependent cytosol-to-membrane translocation of pendrin in rat thyroid PC Cl3 cells.蛋白激酶C-ε依赖性pendrin在大鼠甲状腺PC Cl3细胞中的胞质到膜的转位
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Pendrin, the protein encoded by the Pendred syndrome gene (PDS), is an apical porter of iodide in the thyroid and is regulated by thyroglobulin in FRTL-5 cells.Pendrin是由 Pendred综合征基因(PDS)编码的蛋白质,是甲状腺中碘化物的顶端转运体,在FRTL-5细胞中受甲状腺球蛋白调节。
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Iodine suppression of iodide uptake in FRTL-5 thyroid cells.碘对FRTL-5甲状腺细胞中碘摄取的抑制作用。
Endocrinology. 1986 Jun;118(6):2477-82. doi: 10.1210/endo-118-6-2477.

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