Abstract
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.
Highlights
Iodine is a key ingredient in the synthesis of thyroid hormones and a major factor in the regulation of thyroid function [1, 2]
Western blot was performed to determine the expression of thyroid stimulating hormone receptor (TSHR), TTF-1, and PAX8 in 10 nodular goiter and 10 control thyroid samples. in addition to the increase in TSHR expression, the expressions of TTF-1 and PAX8 in nodular goiter lesions were significantly higher than those in control tissues (Figures 1(a) and 1(b))
TTF-1 and PAX8 were confined to the nucleus of the thyrocytes, and both types of immune reactivity in nodular goiter were significantly higher than those in the control (Figures 2(c), 2(d), 2(e), and 2(f) and Tables 2 and 3)
Summary
Iodine is a key ingredient in the synthesis of thyroid hormones and a major factor in the regulation of thyroid function [1, 2]. Large dose of iodine intake blocks iodine organification and inhibits the synthesis and release of thyroid hormones. This is called the “Wolff-Chaikoff” effect [4, 5]. Iodine has been shown to inhibit multiple signaling pathways of thyroid cells, including CAMP and PIP2. It has been demonstrated that iodinated TG in the follicular lumen can suppress thyroid function and that the suppression takes place through downregulation of TSHR expression in thyroid follicular cells [9,10,11]
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