The Experts below are selected from a list of 174 Experts worldwide ranked by ideXlab platform
Qingyan Cai - One of the best experts on this subject based on the ideXlab platform.
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iodinated tg in thyroid Follicular Lumen regulates ttf 1 and pax8 expression via tsh tshr signaling pathway
Journal of Cellular Biochemistry, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Abstract Our previous study showed that highly iodinated thyroglobulin (TG) inhibited thyroid transcription factor-1 (TTF-1) and paired box gene 8 (PAX8) expression, but the potential mechanism remains unclear. In this study, we constructed a thyroid follicle model in vitro to mimic its natural physiological structure and explored how iodinated TG in the Follicular Lumen tuned TTF-1 and PAX8 expression. Our data showed that lowly iodinated TG enhanced PKA activity while upregulation of both TTF-1 and PAX8 expression; and that highly iodinated TG triggered PKC activity while suppression of TTF-1 and PAX8 expression. Further, PKA agonist alone could increase TTF-1 and PAX8 expression while PKC agonist decreased TTF-1 and PAX8 level. If blocking PLC-PKC pathway using PKC-specific inhibitor, highly iodinated TG significantly promoted the expressions of TTF-1 and PAX8, and similarly PKA-specific blocker moderately inhibited TTF-1 and PAX8 expression. And opposite tendencies of TTF1 and PAX8 aberrant expression were observed in the condition of low iodinated TG when blocking PLC-PKC and cAMP-PKA signaling pathways. Our results indicated that iodinated TG manipulated TTF-1 and PAX8 expression through PLC-PKC and cAMP-PKA pathways, and highly iodinated TG played inhibitory role via PLC-PKC pathway from the TTF1 and PAX8 perspective while low level of iodinated TG was an activator through cAMP-PKA pathway. Our findings proved that iodinated TG in thyroid Follicular Lumen regulated TTF-1 and PAX8 expression through thyroid stimulating hormone/thyroid stimulating hormone receptor (TSH/TSHR) mediated cAMP-PKA and PLC-PKC signaling pathways. J. Cell. Biochem. 118: 3444-3451, 2017. © 2017 Wiley Periodicals, Inc.
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Low Iodine in the Follicular Lumen Caused by Cytoplasm Mis-localization of Sodium Iodide Symporter may Induce Nodular Goiter.
Biological trace element research, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Iodine is a key ingredient in the synthesis of thyroid hormones and also a major factor in the regulation of thyroid function. A local reduction of iodine content in Follicular Lumen leads to overexpression of local thyroid-stimulating hormone receptor (TSHr), which in turn excessively stimulates the regional thyroid tissue, and result in the formation of nodular goiter. In this study, we investigated the relationship between iodine content and sodium iodide symporter (NIS) expression by using the clinical specimens from patients with nodular goiter and explored the pathogenesis triggered by iodine deficiency in nodular goiter. In total, 28 patients were clinically histopathologically confirmed to have nodular goiter and the corresponding adjacent normal thyroid specimens were harvested simultaneously. Western blot and immunohistochemistry were performed to assay NIS expression and localization in thyrocytes of both nodular goiter and adjacent normal thyroid tissues. NIS expression mediated by iodine in Follicular Lumen was confirmed by Follicular model in vitro. Meanwhile, radioscan with iodine-131were conducted on both nodular goiter and adjacent normal thyroid. Our data showed that NIS expression in nodular goiter was significantly higher than that in adjacent normal tissues, which was associated with low iodine in the Follicular Lumen. Abnormal localization of NIS and lower amount of radioactive iodine-131 were also found in nodular goiter. Our data implied that low iodine in the Follicular Lumen caused by cytoplasm mis-localization of NIS may induce nodular goiter.
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Upregulation of TSHR, TTF-1, and PAX8 in Nodular Goiter Is Associated with Iodine Deficiency in the Follicular Lumen
International journal of endocrinology, 2016Co-Authors: Huibin Huang, Lijun Chen, Bo Liang, Huiyao Cai, Qingyan Cai, Yaxiong ShiAbstract: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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Glycolysis-associated enzymes existing in the Follicular Lumen of the thyroid may interfere with energy metabolism
Biomedical reports, 2016Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Honghong Duan, Qingyan CaiAbstract:Synthesis and storage of the thyroid hormone precursor, thyroglobulin (TG), occurs within the Follicular Lumen of the thyroid and the TG is then absorbed into cells for further processing before release into the blood. However, the mechanism of energy metabolism in the Follicular Lumen of the thyroid remains unknown. In the present study, the three dimensional structure of thyroid follicles was constructed using a primary culture of swine cells and the Follicular protein was identified via matrix-assisted laser desorption/ionization-time of flight mass spectrometry. Three glycolysis-associated enzymes, enolase, pyruvate kinase and phosphoglyceraldehyde dehydrogenase were identified in addition to TG. These results support the hypothesis that anaerobic glycolysis of glucose exists in the follicle and supports energy consumption for hormone synthesis.
Yaxiong Shi - One of the best experts on this subject based on the ideXlab platform.
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iodinated tg in thyroid Follicular Lumen regulates ttf 1 and pax8 expression via tsh tshr signaling pathway
Journal of Cellular Biochemistry, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Abstract Our previous study showed that highly iodinated thyroglobulin (TG) inhibited thyroid transcription factor-1 (TTF-1) and paired box gene 8 (PAX8) expression, but the potential mechanism remains unclear. In this study, we constructed a thyroid follicle model in vitro to mimic its natural physiological structure and explored how iodinated TG in the Follicular Lumen tuned TTF-1 and PAX8 expression. Our data showed that lowly iodinated TG enhanced PKA activity while upregulation of both TTF-1 and PAX8 expression; and that highly iodinated TG triggered PKC activity while suppression of TTF-1 and PAX8 expression. Further, PKA agonist alone could increase TTF-1 and PAX8 expression while PKC agonist decreased TTF-1 and PAX8 level. If blocking PLC-PKC pathway using PKC-specific inhibitor, highly iodinated TG significantly promoted the expressions of TTF-1 and PAX8, and similarly PKA-specific blocker moderately inhibited TTF-1 and PAX8 expression. And opposite tendencies of TTF1 and PAX8 aberrant expression were observed in the condition of low iodinated TG when blocking PLC-PKC and cAMP-PKA signaling pathways. Our results indicated that iodinated TG manipulated TTF-1 and PAX8 expression through PLC-PKC and cAMP-PKA pathways, and highly iodinated TG played inhibitory role via PLC-PKC pathway from the TTF1 and PAX8 perspective while low level of iodinated TG was an activator through cAMP-PKA pathway. Our findings proved that iodinated TG in thyroid Follicular Lumen regulated TTF-1 and PAX8 expression through thyroid stimulating hormone/thyroid stimulating hormone receptor (TSH/TSHR) mediated cAMP-PKA and PLC-PKC signaling pathways. J. Cell. Biochem. 118: 3444-3451, 2017. © 2017 Wiley Periodicals, Inc.
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Low Iodine in the Follicular Lumen Caused by Cytoplasm Mis-localization of Sodium Iodide Symporter may Induce Nodular Goiter.
Biological trace element research, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Iodine is a key ingredient in the synthesis of thyroid hormones and also a major factor in the regulation of thyroid function. A local reduction of iodine content in Follicular Lumen leads to overexpression of local thyroid-stimulating hormone receptor (TSHr), which in turn excessively stimulates the regional thyroid tissue, and result in the formation of nodular goiter. In this study, we investigated the relationship between iodine content and sodium iodide symporter (NIS) expression by using the clinical specimens from patients with nodular goiter and explored the pathogenesis triggered by iodine deficiency in nodular goiter. In total, 28 patients were clinically histopathologically confirmed to have nodular goiter and the corresponding adjacent normal thyroid specimens were harvested simultaneously. Western blot and immunohistochemistry were performed to assay NIS expression and localization in thyrocytes of both nodular goiter and adjacent normal thyroid tissues. NIS expression mediated by iodine in Follicular Lumen was confirmed by Follicular model in vitro. Meanwhile, radioscan with iodine-131were conducted on both nodular goiter and adjacent normal thyroid. Our data showed that NIS expression in nodular goiter was significantly higher than that in adjacent normal tissues, which was associated with low iodine in the Follicular Lumen. Abnormal localization of NIS and lower amount of radioactive iodine-131 were also found in nodular goiter. Our data implied that low iodine in the Follicular Lumen caused by cytoplasm mis-localization of NIS may induce nodular goiter.
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Upregulation of TSHR, TTF-1, and PAX8 in Nodular Goiter Is Associated with Iodine Deficiency in the Follicular Lumen
International journal of endocrinology, 2016Co-Authors: Huibin Huang, Lijun Chen, Bo Liang, Huiyao Cai, Qingyan Cai, Yaxiong ShiAbstract: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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Glycolysis-associated enzymes existing in the Follicular Lumen of the thyroid may interfere with energy metabolism
Biomedical reports, 2016Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Honghong Duan, Qingyan CaiAbstract:Synthesis and storage of the thyroid hormone precursor, thyroglobulin (TG), occurs within the Follicular Lumen of the thyroid and the TG is then absorbed into cells for further processing before release into the blood. However, the mechanism of energy metabolism in the Follicular Lumen of the thyroid remains unknown. In the present study, the three dimensional structure of thyroid follicles was constructed using a primary culture of swine cells and the Follicular protein was identified via matrix-assisted laser desorption/ionization-time of flight mass spectrometry. Three glycolysis-associated enzymes, enolase, pyruvate kinase and phosphoglyceraldehyde dehydrogenase were identified in addition to TG. These results support the hypothesis that anaerobic glycolysis of glucose exists in the follicle and supports energy consumption for hormone synthesis.
Huibin Huang - One of the best experts on this subject based on the ideXlab platform.
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iodinated tg in thyroid Follicular Lumen regulates ttf 1 and pax8 expression via tsh tshr signaling pathway
Journal of Cellular Biochemistry, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Abstract Our previous study showed that highly iodinated thyroglobulin (TG) inhibited thyroid transcription factor-1 (TTF-1) and paired box gene 8 (PAX8) expression, but the potential mechanism remains unclear. In this study, we constructed a thyroid follicle model in vitro to mimic its natural physiological structure and explored how iodinated TG in the Follicular Lumen tuned TTF-1 and PAX8 expression. Our data showed that lowly iodinated TG enhanced PKA activity while upregulation of both TTF-1 and PAX8 expression; and that highly iodinated TG triggered PKC activity while suppression of TTF-1 and PAX8 expression. Further, PKA agonist alone could increase TTF-1 and PAX8 expression while PKC agonist decreased TTF-1 and PAX8 level. If blocking PLC-PKC pathway using PKC-specific inhibitor, highly iodinated TG significantly promoted the expressions of TTF-1 and PAX8, and similarly PKA-specific blocker moderately inhibited TTF-1 and PAX8 expression. And opposite tendencies of TTF1 and PAX8 aberrant expression were observed in the condition of low iodinated TG when blocking PLC-PKC and cAMP-PKA signaling pathways. Our results indicated that iodinated TG manipulated TTF-1 and PAX8 expression through PLC-PKC and cAMP-PKA pathways, and highly iodinated TG played inhibitory role via PLC-PKC pathway from the TTF1 and PAX8 perspective while low level of iodinated TG was an activator through cAMP-PKA pathway. Our findings proved that iodinated TG in thyroid Follicular Lumen regulated TTF-1 and PAX8 expression through thyroid stimulating hormone/thyroid stimulating hormone receptor (TSH/TSHR) mediated cAMP-PKA and PLC-PKC signaling pathways. J. Cell. Biochem. 118: 3444-3451, 2017. © 2017 Wiley Periodicals, Inc.
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Low Iodine in the Follicular Lumen Caused by Cytoplasm Mis-localization of Sodium Iodide Symporter may Induce Nodular Goiter.
Biological trace element research, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Iodine is a key ingredient in the synthesis of thyroid hormones and also a major factor in the regulation of thyroid function. A local reduction of iodine content in Follicular Lumen leads to overexpression of local thyroid-stimulating hormone receptor (TSHr), which in turn excessively stimulates the regional thyroid tissue, and result in the formation of nodular goiter. In this study, we investigated the relationship between iodine content and sodium iodide symporter (NIS) expression by using the clinical specimens from patients with nodular goiter and explored the pathogenesis triggered by iodine deficiency in nodular goiter. In total, 28 patients were clinically histopathologically confirmed to have nodular goiter and the corresponding adjacent normal thyroid specimens were harvested simultaneously. Western blot and immunohistochemistry were performed to assay NIS expression and localization in thyrocytes of both nodular goiter and adjacent normal thyroid tissues. NIS expression mediated by iodine in Follicular Lumen was confirmed by Follicular model in vitro. Meanwhile, radioscan with iodine-131were conducted on both nodular goiter and adjacent normal thyroid. Our data showed that NIS expression in nodular goiter was significantly higher than that in adjacent normal tissues, which was associated with low iodine in the Follicular Lumen. Abnormal localization of NIS and lower amount of radioactive iodine-131 were also found in nodular goiter. Our data implied that low iodine in the Follicular Lumen caused by cytoplasm mis-localization of NIS may induce nodular goiter.
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Upregulation of TSHR, TTF-1, and PAX8 in Nodular Goiter Is Associated with Iodine Deficiency in the Follicular Lumen
International journal of endocrinology, 2016Co-Authors: Huibin Huang, Lijun Chen, Bo Liang, Huiyao Cai, Qingyan Cai, Yaxiong ShiAbstract: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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Glycolysis-associated enzymes existing in the Follicular Lumen of the thyroid may interfere with energy metabolism
Biomedical reports, 2016Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Honghong Duan, Qingyan CaiAbstract:Synthesis and storage of the thyroid hormone precursor, thyroglobulin (TG), occurs within the Follicular Lumen of the thyroid and the TG is then absorbed into cells for further processing before release into the blood. However, the mechanism of energy metabolism in the Follicular Lumen of the thyroid remains unknown. In the present study, the three dimensional structure of thyroid follicles was constructed using a primary culture of swine cells and the Follicular protein was identified via matrix-assisted laser desorption/ionization-time of flight mass spectrometry. Three glycolysis-associated enzymes, enolase, pyruvate kinase and phosphoglyceraldehyde dehydrogenase were identified in addition to TG. These results support the hypothesis that anaerobic glycolysis of glucose exists in the follicle and supports energy consumption for hormone synthesis.
Huiyao Cai - One of the best experts on this subject based on the ideXlab platform.
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iodinated tg in thyroid Follicular Lumen regulates ttf 1 and pax8 expression via tsh tshr signaling pathway
Journal of Cellular Biochemistry, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Abstract Our previous study showed that highly iodinated thyroglobulin (TG) inhibited thyroid transcription factor-1 (TTF-1) and paired box gene 8 (PAX8) expression, but the potential mechanism remains unclear. In this study, we constructed a thyroid follicle model in vitro to mimic its natural physiological structure and explored how iodinated TG in the Follicular Lumen tuned TTF-1 and PAX8 expression. Our data showed that lowly iodinated TG enhanced PKA activity while upregulation of both TTF-1 and PAX8 expression; and that highly iodinated TG triggered PKC activity while suppression of TTF-1 and PAX8 expression. Further, PKA agonist alone could increase TTF-1 and PAX8 expression while PKC agonist decreased TTF-1 and PAX8 level. If blocking PLC-PKC pathway using PKC-specific inhibitor, highly iodinated TG significantly promoted the expressions of TTF-1 and PAX8, and similarly PKA-specific blocker moderately inhibited TTF-1 and PAX8 expression. And opposite tendencies of TTF1 and PAX8 aberrant expression were observed in the condition of low iodinated TG when blocking PLC-PKC and cAMP-PKA signaling pathways. Our results indicated that iodinated TG manipulated TTF-1 and PAX8 expression through PLC-PKC and cAMP-PKA pathways, and highly iodinated TG played inhibitory role via PLC-PKC pathway from the TTF1 and PAX8 perspective while low level of iodinated TG was an activator through cAMP-PKA pathway. Our findings proved that iodinated TG in thyroid Follicular Lumen regulated TTF-1 and PAX8 expression through thyroid stimulating hormone/thyroid stimulating hormone receptor (TSH/TSHR) mediated cAMP-PKA and PLC-PKC signaling pathways. J. Cell. Biochem. 118: 3444-3451, 2017. © 2017 Wiley Periodicals, Inc.
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Low Iodine in the Follicular Lumen Caused by Cytoplasm Mis-localization of Sodium Iodide Symporter may Induce Nodular Goiter.
Biological trace element research, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Iodine is a key ingredient in the synthesis of thyroid hormones and also a major factor in the regulation of thyroid function. A local reduction of iodine content in Follicular Lumen leads to overexpression of local thyroid-stimulating hormone receptor (TSHr), which in turn excessively stimulates the regional thyroid tissue, and result in the formation of nodular goiter. In this study, we investigated the relationship between iodine content and sodium iodide symporter (NIS) expression by using the clinical specimens from patients with nodular goiter and explored the pathogenesis triggered by iodine deficiency in nodular goiter. In total, 28 patients were clinically histopathologically confirmed to have nodular goiter and the corresponding adjacent normal thyroid specimens were harvested simultaneously. Western blot and immunohistochemistry were performed to assay NIS expression and localization in thyrocytes of both nodular goiter and adjacent normal thyroid tissues. NIS expression mediated by iodine in Follicular Lumen was confirmed by Follicular model in vitro. Meanwhile, radioscan with iodine-131were conducted on both nodular goiter and adjacent normal thyroid. Our data showed that NIS expression in nodular goiter was significantly higher than that in adjacent normal tissues, which was associated with low iodine in the Follicular Lumen. Abnormal localization of NIS and lower amount of radioactive iodine-131 were also found in nodular goiter. Our data implied that low iodine in the Follicular Lumen caused by cytoplasm mis-localization of NIS may induce nodular goiter.
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Upregulation of TSHR, TTF-1, and PAX8 in Nodular Goiter Is Associated with Iodine Deficiency in the Follicular Lumen
International journal of endocrinology, 2016Co-Authors: Huibin Huang, Lijun Chen, Bo Liang, Huiyao Cai, Qingyan Cai, Yaxiong ShiAbstract: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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Glycolysis-associated enzymes existing in the Follicular Lumen of the thyroid may interfere with energy metabolism
Biomedical reports, 2016Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Honghong Duan, Qingyan CaiAbstract:Synthesis and storage of the thyroid hormone precursor, thyroglobulin (TG), occurs within the Follicular Lumen of the thyroid and the TG is then absorbed into cells for further processing before release into the blood. However, the mechanism of energy metabolism in the Follicular Lumen of the thyroid remains unknown. In the present study, the three dimensional structure of thyroid follicles was constructed using a primary culture of swine cells and the Follicular protein was identified via matrix-assisted laser desorption/ionization-time of flight mass spectrometry. Three glycolysis-associated enzymes, enolase, pyruvate kinase and phosphoglyceraldehyde dehydrogenase were identified in addition to TG. These results support the hypothesis that anaerobic glycolysis of glucose exists in the follicle and supports energy consumption for hormone synthesis.
Bo Liang - One of the best experts on this subject based on the ideXlab platform.
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iodinated tg in thyroid Follicular Lumen regulates ttf 1 and pax8 expression via tsh tshr signaling pathway
Journal of Cellular Biochemistry, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Abstract Our previous study showed that highly iodinated thyroglobulin (TG) inhibited thyroid transcription factor-1 (TTF-1) and paired box gene 8 (PAX8) expression, but the potential mechanism remains unclear. In this study, we constructed a thyroid follicle model in vitro to mimic its natural physiological structure and explored how iodinated TG in the Follicular Lumen tuned TTF-1 and PAX8 expression. Our data showed that lowly iodinated TG enhanced PKA activity while upregulation of both TTF-1 and PAX8 expression; and that highly iodinated TG triggered PKC activity while suppression of TTF-1 and PAX8 expression. Further, PKA agonist alone could increase TTF-1 and PAX8 expression while PKC agonist decreased TTF-1 and PAX8 level. If blocking PLC-PKC pathway using PKC-specific inhibitor, highly iodinated TG significantly promoted the expressions of TTF-1 and PAX8, and similarly PKA-specific blocker moderately inhibited TTF-1 and PAX8 expression. And opposite tendencies of TTF1 and PAX8 aberrant expression were observed in the condition of low iodinated TG when blocking PLC-PKC and cAMP-PKA signaling pathways. Our results indicated that iodinated TG manipulated TTF-1 and PAX8 expression through PLC-PKC and cAMP-PKA pathways, and highly iodinated TG played inhibitory role via PLC-PKC pathway from the TTF1 and PAX8 perspective while low level of iodinated TG was an activator through cAMP-PKA pathway. Our findings proved that iodinated TG in thyroid Follicular Lumen regulated TTF-1 and PAX8 expression through thyroid stimulating hormone/thyroid stimulating hormone receptor (TSH/TSHR) mediated cAMP-PKA and PLC-PKC signaling pathways. J. Cell. Biochem. 118: 3444-3451, 2017. © 2017 Wiley Periodicals, Inc.
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Low Iodine in the Follicular Lumen Caused by Cytoplasm Mis-localization of Sodium Iodide Symporter may Induce Nodular Goiter.
Biological trace element research, 2017Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Qingyan CaiAbstract:Iodine is a key ingredient in the synthesis of thyroid hormones and also a major factor in the regulation of thyroid function. A local reduction of iodine content in Follicular Lumen leads to overexpression of local thyroid-stimulating hormone receptor (TSHr), which in turn excessively stimulates the regional thyroid tissue, and result in the formation of nodular goiter. In this study, we investigated the relationship between iodine content and sodium iodide symporter (NIS) expression by using the clinical specimens from patients with nodular goiter and explored the pathogenesis triggered by iodine deficiency in nodular goiter. In total, 28 patients were clinically histopathologically confirmed to have nodular goiter and the corresponding adjacent normal thyroid specimens were harvested simultaneously. Western blot and immunohistochemistry were performed to assay NIS expression and localization in thyrocytes of both nodular goiter and adjacent normal thyroid tissues. NIS expression mediated by iodine in Follicular Lumen was confirmed by Follicular model in vitro. Meanwhile, radioscan with iodine-131were conducted on both nodular goiter and adjacent normal thyroid. Our data showed that NIS expression in nodular goiter was significantly higher than that in adjacent normal tissues, which was associated with low iodine in the Follicular Lumen. Abnormal localization of NIS and lower amount of radioactive iodine-131 were also found in nodular goiter. Our data implied that low iodine in the Follicular Lumen caused by cytoplasm mis-localization of NIS may induce nodular goiter.
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Upregulation of TSHR, TTF-1, and PAX8 in Nodular Goiter Is Associated with Iodine Deficiency in the Follicular Lumen
International journal of endocrinology, 2016Co-Authors: Huibin Huang, Lijun Chen, Bo Liang, Huiyao Cai, Qingyan Cai, Yaxiong ShiAbstract: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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Glycolysis-associated enzymes existing in the Follicular Lumen of the thyroid may interfere with energy metabolism
Biomedical reports, 2016Co-Authors: Huibin Huang, Bo Liang, Huiyao Cai, Yaxiong Shi, Honghong Duan, Qingyan CaiAbstract:Synthesis and storage of the thyroid hormone precursor, thyroglobulin (TG), occurs within the Follicular Lumen of the thyroid and the TG is then absorbed into cells for further processing before release into the blood. However, the mechanism of energy metabolism in the Follicular Lumen of the thyroid remains unknown. In the present study, the three dimensional structure of thyroid follicles was constructed using a primary culture of swine cells and the Follicular protein was identified via matrix-assisted laser desorption/ionization-time of flight mass spectrometry. Three glycolysis-associated enzymes, enolase, pyruvate kinase and phosphoglyceraldehyde dehydrogenase were identified in addition to TG. These results support the hypothesis that anaerobic glycolysis of glucose exists in the follicle and supports energy consumption for hormone synthesis.