Molecular mechanisms of human thyrocyte dysfunction induced by low concentrations of polychlorinated biphenyl 118 through the Akt/FoxO3a/NIS pathway
ABSTRACT Polychlorinated biphenyls (PCBs) are typical persistent organic pollutants that can interfere with multiple organ systems of humans. Previously, we concluded that persistent exposure to low doses of PCB118 could severely damage the thyroidal structure, dramatically decrease the concentratio...
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| Veröffentlicht in: | Journal of applied toxicology 2015-09, Vol.35 (9), p.992-998 |
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| creator | Guo, Hongwei Yang, Hui Chen, Huanhuan Li, Wen Tang, Jinmei Cheng, Pei Xie, Yuchun Liu, Yun Ding, Guoxian Cui, Dai Zheng, Xuqin Duan, Yu |
| description | ABSTRACT
Polychlorinated biphenyls (PCBs) are typical persistent organic pollutants that can interfere with multiple organ systems of humans. Previously, we concluded that persistent exposure to low doses of PCB118 could severely damage the thyroidal structure, dramatically decrease the concentration of serum thyroid hormones and inhibit the pivotal gene expressions such as sodium/iodide symporter (NIS) and thyroglobulin (Tg). To explore the molecular mechanisms of thyrocyte dysfunction induced by 2,3′,4,4′,5‐pentachlorobiphenyl (PCB118), monolayer cultured human thyroid epithelial cells (HTECs) were treated with PCB118 or dimethyl sulfoxide (DMSO) as a control. Our results indicated that relatively higher concentrations of PCB118 could induce a loss in the viability of HTEC. In cultures with concentrations of PCB118 from 0.025 to 25 nM, which did not affect cell viability or apoptosis, concentrations of Tg and thyroxine (T4) were significantly decreased compared with those in the controls. In addition, mRNA and protein levels of Akt were increased significantly in the PCB118‐treated groups, whereas FoxO3a expression did not show particular variation. Furthermore, exposure to PCB118 was associated with a significant increase of the protein levels of p‐Akt and p‐FoxO3a, and these effects were blocked by LY294002. In contrast, mRNA and protein expression levels of NIS were decreased significantly, and this effect was blocked by LY294002. Unlike control cells, a cytoplasmic shift of FoxO3a was observed in the PCB118‐treated group. Our research suggests that PCB118 may induce thyrocyte dysfunction through the Akt/FoxO3a/NIS signalling pathway, which provides potential new insights for finding interventions to counteract the damage to the human body caused by PCBs. Copyright © 2015 John Wiley & Sons, Ltd.
Related protein and gene expression levels were observed in a low dose of 2,3′,4,4′,5‐pentachlorobiphenyl (PCB118)‐exposed human thyroid epithelial cells. We concluded that a low dose of PCB118 could activate the PI3k/Akt pathway, increase the phosphorylation level of FoxO3a protein, and decrease the protein and gene expression level of sodium/iodide symporter (NIS). Our results suggest that PCB118 may induce thyrocyte dysfunction through the Akt/FoxO3a/NIS signalling pathway. |
| doi_str_mv | 10.1002/jat.3032 |
| format | Article |
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Polychlorinated biphenyls (PCBs) are typical persistent organic pollutants that can interfere with multiple organ systems of humans. Previously, we concluded that persistent exposure to low doses of PCB118 could severely damage the thyroidal structure, dramatically decrease the concentration of serum thyroid hormones and inhibit the pivotal gene expressions such as sodium/iodide symporter (NIS) and thyroglobulin (Tg). To explore the molecular mechanisms of thyrocyte dysfunction induced by 2,3′,4,4′,5‐pentachlorobiphenyl (PCB118), monolayer cultured human thyroid epithelial cells (HTECs) were treated with PCB118 or dimethyl sulfoxide (DMSO) as a control. Our results indicated that relatively higher concentrations of PCB118 could induce a loss in the viability of HTEC. In cultures with concentrations of PCB118 from 0.025 to 25 nM, which did not affect cell viability or apoptosis, concentrations of Tg and thyroxine (T4) were significantly decreased compared with those in the controls. In addition, mRNA and protein levels of Akt were increased significantly in the PCB118‐treated groups, whereas FoxO3a expression did not show particular variation. Furthermore, exposure to PCB118 was associated with a significant increase of the protein levels of p‐Akt and p‐FoxO3a, and these effects were blocked by LY294002. In contrast, mRNA and protein expression levels of NIS were decreased significantly, and this effect was blocked by LY294002. Unlike control cells, a cytoplasmic shift of FoxO3a was observed in the PCB118‐treated group. Our research suggests that PCB118 may induce thyrocyte dysfunction through the Akt/FoxO3a/NIS signalling pathway, which provides potential new insights for finding interventions to counteract the damage to the human body caused by PCBs. Copyright © 2015 John Wiley & Sons, Ltd.
Related protein and gene expression levels were observed in a low dose of 2,3′,4,4′,5‐pentachlorobiphenyl (PCB118)‐exposed human thyroid epithelial cells. We concluded that a low dose of PCB118 could activate the PI3k/Akt pathway, increase the phosphorylation level of FoxO3a protein, and decrease the protein and gene expression level of sodium/iodide symporter (NIS). Our results suggest that PCB118 may induce thyrocyte dysfunction through the Akt/FoxO3a/NIS signalling pathway.</description><identifier>ISSN: 0260-437X</identifier><identifier>EISSN: 1099-1263</identifier><identifier>DOI: 10.1002/jat.3032</identifier><identifier>PMID: 25644787</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Apoptosis - drug effects ; Blotting, Western ; Cell Survival - drug effects ; Cells, Cultured ; Damage ; Environmental Pollutants - toxicity ; Epithelial Cells - drug effects ; Epithelial Cells - enzymology ; Epithelial Cells - pathology ; Forkhead Box Protein O3 ; Forkhead Transcription Factors - metabolism ; FoxO3a ; Gene expression ; Human ; Humans ; NIS ; Pathways ; PCB ; PI3K/Akt ; Polychlorinated biphenyls ; Polychlorinated Biphenyls - toxicity ; Polychlorinated biphenyls 118 ; Primary Cell Culture ; Protein expression ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Real-Time Polymerase Chain Reaction ; Signal Transduction ; Signalling ; Sodium ; Symporters - metabolism ; thyrocyte dysfunction ; Thyroid Gland - drug effects ; Thyroid Gland - enzymology ; Thyroid Gland - pathology ; Toxicology ; Viability</subject><ispartof>Journal of applied toxicology, 2015-09, Vol.35 (9), p.992-998</ispartof><rights>Copyright © 2015 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5192-7d7735997fff33ff6e3c88ed07f3c5aa441e428e8e1fdff64be46924e14923223</citedby><cites>FETCH-LOGICAL-c5192-7d7735997fff33ff6e3c88ed07f3c5aa441e428e8e1fdff64be46924e14923223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjat.3032$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjat.3032$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25644787$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Hongwei</creatorcontrib><creatorcontrib>Yang, Hui</creatorcontrib><creatorcontrib>Chen, Huanhuan</creatorcontrib><creatorcontrib>Li, Wen</creatorcontrib><creatorcontrib>Tang, Jinmei</creatorcontrib><creatorcontrib>Cheng, Pei</creatorcontrib><creatorcontrib>Xie, Yuchun</creatorcontrib><creatorcontrib>Liu, Yun</creatorcontrib><creatorcontrib>Ding, Guoxian</creatorcontrib><creatorcontrib>Cui, Dai</creatorcontrib><creatorcontrib>Zheng, Xuqin</creatorcontrib><creatorcontrib>Duan, Yu</creatorcontrib><title>Molecular mechanisms of human thyrocyte dysfunction induced by low concentrations of polychlorinated biphenyl 118 through the Akt/FoxO3a/NIS pathway</title><title>Journal of applied toxicology</title><addtitle>J. Appl. Toxicol</addtitle><description>ABSTRACT
Polychlorinated biphenyls (PCBs) are typical persistent organic pollutants that can interfere with multiple organ systems of humans. Previously, we concluded that persistent exposure to low doses of PCB118 could severely damage the thyroidal structure, dramatically decrease the concentration of serum thyroid hormones and inhibit the pivotal gene expressions such as sodium/iodide symporter (NIS) and thyroglobulin (Tg). To explore the molecular mechanisms of thyrocyte dysfunction induced by 2,3′,4,4′,5‐pentachlorobiphenyl (PCB118), monolayer cultured human thyroid epithelial cells (HTECs) were treated with PCB118 or dimethyl sulfoxide (DMSO) as a control. Our results indicated that relatively higher concentrations of PCB118 could induce a loss in the viability of HTEC. In cultures with concentrations of PCB118 from 0.025 to 25 nM, which did not affect cell viability or apoptosis, concentrations of Tg and thyroxine (T4) were significantly decreased compared with those in the controls. In addition, mRNA and protein levels of Akt were increased significantly in the PCB118‐treated groups, whereas FoxO3a expression did not show particular variation. Furthermore, exposure to PCB118 was associated with a significant increase of the protein levels of p‐Akt and p‐FoxO3a, and these effects were blocked by LY294002. In contrast, mRNA and protein expression levels of NIS were decreased significantly, and this effect was blocked by LY294002. Unlike control cells, a cytoplasmic shift of FoxO3a was observed in the PCB118‐treated group. Our research suggests that PCB118 may induce thyrocyte dysfunction through the Akt/FoxO3a/NIS signalling pathway, which provides potential new insights for finding interventions to counteract the damage to the human body caused by PCBs. Copyright © 2015 John Wiley & Sons, Ltd.
Related protein and gene expression levels were observed in a low dose of 2,3′,4,4′,5‐pentachlorobiphenyl (PCB118)‐exposed human thyroid epithelial cells. We concluded that a low dose of PCB118 could activate the PI3k/Akt pathway, increase the phosphorylation level of FoxO3a protein, and decrease the protein and gene expression level of sodium/iodide symporter (NIS). Our results suggest that PCB118 may induce thyrocyte dysfunction through the Akt/FoxO3a/NIS signalling pathway.</description><subject>Apoptosis - drug effects</subject><subject>Blotting, Western</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Damage</subject><subject>Environmental Pollutants - toxicity</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - enzymology</subject><subject>Epithelial Cells - pathology</subject><subject>Forkhead Box Protein O3</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>FoxO3a</subject><subject>Gene expression</subject><subject>Human</subject><subject>Humans</subject><subject>NIS</subject><subject>Pathways</subject><subject>PCB</subject><subject>PI3K/Akt</subject><subject>Polychlorinated biphenyls</subject><subject>Polychlorinated Biphenyls - toxicity</subject><subject>Polychlorinated biphenyls 118</subject><subject>Primary Cell Culture</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Signal Transduction</subject><subject>Signalling</subject><subject>Sodium</subject><subject>Symporters - metabolism</subject><subject>thyrocyte dysfunction</subject><subject>Thyroid Gland - drug effects</subject><subject>Thyroid Gland - enzymology</subject><subject>Thyroid Gland - pathology</subject><subject>Toxicology</subject><subject>Viability</subject><issn>0260-437X</issn><issn>1099-1263</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhSMEokNB4gmQJTZs0vFfYns5qujQqrQSU1R2lse5Jpkm9mAnmuY9eOBm6FAkJCRWZ3G--0lXJ8veEnxCMKbzjelPGGb0WTYjWKmc0JI9z2aYljjnTHw7yl6ltMF46qh8mR3RouRcSDHLfn4OLdihNRF1YGvjm9QlFByqh8541NdjDHbsAVVjcoO3fRM8anw1WKjQekRt2CEbvAXfR7Mvfx1vQzvaug2x8abfg822Bj-2iBA5OWMYvtdTAlrc9fOzcH_NzPzqfIW2pq93ZnydvXCmTfDmkMfZ17OPN6ef8svr5fnp4jK3BVE0F5UQrFBKOOcYc64EZqWECgvHbGEM5wQ4lSCBuGqq-Rp4qSgHwhVllLLj7MOjdxvDjwFSr7smWWhb4yEMSRNBpBJFKf8HxQVWmBI2oe__QjdhiH56RJNSSYU5K8o_QhtDShGc3samM3HUBOv9qHoaVe9HndB3B-Gw7qB6An-vOAH5I7BrWhj_KdIXi5uD8MA3qYf7J97EO10KJgp9e7XUYsVWt8svQq_YAw_-u3k</recordid><startdate>201509</startdate><enddate>201509</enddate><creator>Guo, Hongwei</creator><creator>Yang, Hui</creator><creator>Chen, Huanhuan</creator><creator>Li, Wen</creator><creator>Tang, Jinmei</creator><creator>Cheng, Pei</creator><creator>Xie, Yuchun</creator><creator>Liu, Yun</creator><creator>Ding, Guoxian</creator><creator>Cui, Dai</creator><creator>Zheng, Xuqin</creator><creator>Duan, Yu</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7ST</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>SOI</scope><scope>7TV</scope><scope>8FD</scope><scope>FR3</scope><scope>KR7</scope></search><sort><creationdate>201509</creationdate><title>Molecular mechanisms of human thyrocyte dysfunction induced by low concentrations of polychlorinated biphenyl 118 through the Akt/FoxO3a/NIS pathway</title><author>Guo, Hongwei ; Yang, Hui ; Chen, Huanhuan ; Li, Wen ; Tang, Jinmei ; Cheng, Pei ; Xie, Yuchun ; Liu, Yun ; Ding, Guoxian ; Cui, Dai ; Zheng, Xuqin ; Duan, Yu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5192-7d7735997fff33ff6e3c88ed07f3c5aa441e428e8e1fdff64be46924e14923223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Apoptosis - drug effects</topic><topic>Blotting, Western</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Damage</topic><topic>Environmental Pollutants - toxicity</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - enzymology</topic><topic>Epithelial Cells - pathology</topic><topic>Forkhead Box Protein O3</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>FoxO3a</topic><topic>Gene expression</topic><topic>Human</topic><topic>Humans</topic><topic>NIS</topic><topic>Pathways</topic><topic>PCB</topic><topic>PI3K/Akt</topic><topic>Polychlorinated biphenyls</topic><topic>Polychlorinated Biphenyls - toxicity</topic><topic>Polychlorinated biphenyls 118</topic><topic>Primary Cell Culture</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Signal Transduction</topic><topic>Signalling</topic><topic>Sodium</topic><topic>Symporters - metabolism</topic><topic>thyrocyte dysfunction</topic><topic>Thyroid Gland - drug effects</topic><topic>Thyroid Gland - enzymology</topic><topic>Thyroid Gland - pathology</topic><topic>Toxicology</topic><topic>Viability</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Hongwei</creatorcontrib><creatorcontrib>Yang, Hui</creatorcontrib><creatorcontrib>Chen, Huanhuan</creatorcontrib><creatorcontrib>Li, Wen</creatorcontrib><creatorcontrib>Tang, Jinmei</creatorcontrib><creatorcontrib>Cheng, Pei</creatorcontrib><creatorcontrib>Xie, Yuchun</creatorcontrib><creatorcontrib>Liu, Yun</creatorcontrib><creatorcontrib>Ding, Guoxian</creatorcontrib><creatorcontrib>Cui, Dai</creatorcontrib><creatorcontrib>Zheng, Xuqin</creatorcontrib><creatorcontrib>Duan, Yu</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Environment Abstracts</collection><collection>Pollution Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Civil Engineering Abstracts</collection><jtitle>Journal of applied toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Hongwei</au><au>Yang, Hui</au><au>Chen, Huanhuan</au><au>Li, Wen</au><au>Tang, Jinmei</au><au>Cheng, Pei</au><au>Xie, Yuchun</au><au>Liu, Yun</au><au>Ding, Guoxian</au><au>Cui, Dai</au><au>Zheng, Xuqin</au><au>Duan, Yu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular mechanisms of human thyrocyte dysfunction induced by low concentrations of polychlorinated biphenyl 118 through the Akt/FoxO3a/NIS pathway</atitle><jtitle>Journal of applied toxicology</jtitle><addtitle>J. Appl. Toxicol</addtitle><date>2015-09</date><risdate>2015</risdate><volume>35</volume><issue>9</issue><spage>992</spage><epage>998</epage><pages>992-998</pages><issn>0260-437X</issn><eissn>1099-1263</eissn><abstract>ABSTRACT
Polychlorinated biphenyls (PCBs) are typical persistent organic pollutants that can interfere with multiple organ systems of humans. Previously, we concluded that persistent exposure to low doses of PCB118 could severely damage the thyroidal structure, dramatically decrease the concentration of serum thyroid hormones and inhibit the pivotal gene expressions such as sodium/iodide symporter (NIS) and thyroglobulin (Tg). To explore the molecular mechanisms of thyrocyte dysfunction induced by 2,3′,4,4′,5‐pentachlorobiphenyl (PCB118), monolayer cultured human thyroid epithelial cells (HTECs) were treated with PCB118 or dimethyl sulfoxide (DMSO) as a control. Our results indicated that relatively higher concentrations of PCB118 could induce a loss in the viability of HTEC. In cultures with concentrations of PCB118 from 0.025 to 25 nM, which did not affect cell viability or apoptosis, concentrations of Tg and thyroxine (T4) were significantly decreased compared with those in the controls. In addition, mRNA and protein levels of Akt were increased significantly in the PCB118‐treated groups, whereas FoxO3a expression did not show particular variation. Furthermore, exposure to PCB118 was associated with a significant increase of the protein levels of p‐Akt and p‐FoxO3a, and these effects were blocked by LY294002. In contrast, mRNA and protein expression levels of NIS were decreased significantly, and this effect was blocked by LY294002. Unlike control cells, a cytoplasmic shift of FoxO3a was observed in the PCB118‐treated group. Our research suggests that PCB118 may induce thyrocyte dysfunction through the Akt/FoxO3a/NIS signalling pathway, which provides potential new insights for finding interventions to counteract the damage to the human body caused by PCBs. Copyright © 2015 John Wiley & Sons, Ltd.
Related protein and gene expression levels were observed in a low dose of 2,3′,4,4′,5‐pentachlorobiphenyl (PCB118)‐exposed human thyroid epithelial cells. We concluded that a low dose of PCB118 could activate the PI3k/Akt pathway, increase the phosphorylation level of FoxO3a protein, and decrease the protein and gene expression level of sodium/iodide symporter (NIS). Our results suggest that PCB118 may induce thyrocyte dysfunction through the Akt/FoxO3a/NIS signalling pathway.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>25644787</pmid><doi>10.1002/jat.3032</doi><tpages>7</tpages></addata></record> |
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| subjects | Apoptosis - drug effects Blotting, Western Cell Survival - drug effects Cells, Cultured Damage Environmental Pollutants - toxicity Epithelial Cells - drug effects Epithelial Cells - enzymology Epithelial Cells - pathology Forkhead Box Protein O3 Forkhead Transcription Factors - metabolism FoxO3a Gene expression Human Humans NIS Pathways PCB PI3K/Akt Polychlorinated biphenyls Polychlorinated Biphenyls - toxicity Polychlorinated biphenyls 118 Primary Cell Culture Protein expression Proteins Proto-Oncogene Proteins c-akt - metabolism Real-Time Polymerase Chain Reaction Signal Transduction Signalling Sodium Symporters - metabolism thyrocyte dysfunction Thyroid Gland - drug effects Thyroid Gland - enzymology Thyroid Gland - pathology Toxicology Viability |
| title | Molecular mechanisms of human thyrocyte dysfunction induced by low concentrations of polychlorinated biphenyl 118 through the Akt/FoxO3a/NIS pathway |
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