title: Excess iodine promotes apoptosis of thyroid follicular epithelial cells by inducing autophagy suppression and is associated with Hashimoto thyroiditis disease.
abstract: The incidence of the autoimmune thyroid disease Hashimoto thyroiditis (HT) has increased in recent years, and increasing evidence supports the contribution of excess iodine intake to thyroid disease. In this study, we examined the status of autophagy and apoptosis in thyroid tissues obtained from patients with HT, and we determined the effects of excessive iodine on the autophagy and apoptosis of thyroid follicular cells (TFCs) in an attempt to elucidate the effects of excess iodine on HT development. Our results showed decreases in the autophagy-related protein LC3B-II, and increases in caspase-3 were observed in thyroid tissues from HT patients. Interestingly, the suppression of autophagy activity in TFCs was induced by excess iodine in vitro, and this process is mediated through transforming growth factor-β1 downregulation and activation of the Akt/mTOR signaling pathway. In addition, excess iodine induced autophagy suppression and enhanced reactive oxygen species (ROS) production and apoptosis of TFCs, which could be rescued by the activation of autophagy. Taken together, our results demonstrated that excess iodine contributed to autophagy suppression and apoptosis of TFCs, which could be important factors predisposing to increased risk of HT development.
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
authors.forename: Chengcheng
authors.initials: C
authors.lastname: Xu
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
authors.forename: Fei
authors.initials: F
authors.lastname: Wu
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China. Electronic address: jq1001@ujs.edu.cn.
authors.forename: Chaoming
authors.initials: C
authors.lastname: Mao
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
authors.forename: Xuefeng
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
authors.forename: Tingting
authors.initials: T
authors.lastname: Zheng
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Bu
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Mou
authors.affiliation: Institute of Oncology, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
authors.forename: Yuepeng
authors.initials: Y
authors.lastname: Zhou
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China.
authors.forename: Guoyue
authors.initials: G
authors.lastname: Yuan
authors.affiliation: Department of Laboratory Immunology, Jiangsu University School of Medicine, Zhenjiang 212001, China.
authors.forename: Shengjun
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, 438 Jiefang Road, Zhenjiang 212001, China; Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. Electronic address: ycxiao@sibs.ac.cn.
authors.forename: Yichuan
authors.initials: Y
authors.lastname: Xiao
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000903:Antibiotics, Antineoplastic / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology*; D001343:Autophagy / Q000187:drug effects / Q000276:immunology*; D000071183:Autophagy-Related Proteins / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D002460:Cell Line; D004847:Epithelial Cells / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D050031:Hashimoto Disease / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D015151:Immunoblotting; D007150:Immunohistochemistry; D007455:Iodine / Q000276:immunology* / Q000378:metabolism / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000276:immunology / Q000378:metabolism; D020123:Sirolimus / Q000494:pharmacology; D013961:Thyroid Gland / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology
chemical_list: D000903:Antibiotics, Antineoplastic; D000071183:Autophagy-Related Proteins; D017382:Reactive Oxygen Species; D053773:Transforming Growth Factor beta1; D007455:Iodine; D053148:Caspase 3; D020123:Sirolimus; D000111:Acetylcysteine
keywords: Apoptosis; Autophagy; Excess iodine; Hashimoto thyroiditis; Reactive oxygen species