Excess iodine promotes apoptosis of thyroid follicular epithelial cells by inducing autophagy suppression and is associated with Hashimoto thyroiditis disease

Excess iodine promotes apoptosis of thyroid follicular epithelial cells by inducing autophagy suppression and is associated with Hashimoto thyroiditis disease
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过量碘通过诱导自噬抑制促进甲状腺滤泡上皮细胞凋亡,并与桥本甲状腺炎相关

DOI:
10.1016/j.jaut.2016.07.008
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发表时间:
2016-12-01
影响因子:
12.8
通讯作者:
Xiao, Yichuan
Xiao, Yichuan
中科院分区:
医学1区
文献类型:
--
作者:
Xu, Chengcheng;Wu, Fei;Xiao, Yichuan

文献摘要

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近年来,自身免疫性甲状腺疾病桥本甲状腺炎(HT)的发病率有所增加,越来越多的证据支持过量碘摄入对甲状腺疾病的贡献。在这项研究中,我们研究了甲状腺组织中的自噬和凋亡的状态,从HT患者,我们确定了过量碘对甲状腺滤泡细胞(TFCs)的自噬和凋亡的影响,试图阐明过量碘对HT发展的影响。我们的研究结果表明,自噬相关蛋白LC 3B-II的减少,并增加半胱天冬酶-3在甲状腺组织中观察到HT患者。有趣的是,体外过量碘诱导了TFCs中自噬活性的抑制,并且该过程通过转化生长因子β 1和Akt/mTOR信号传导途径的激活介导。此外,过量碘诱导自噬抑制,增加活性氧(ROS)的产生和TFCs的凋亡,这可以通过激活自噬来拯救。总之,我们的研究结果表明,过量的碘有助于TFCs的自噬抑制和凋亡,这可能是导致HT发展风险增加的重要因素。(C)2016爱思唯尔有限公司版权所有
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 (31 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. (C) 2016 Elsevier Ltd. All rights reserved.