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

Xu, Chengcheng; Wu, Fei; Mao, Chaoming; Wang, Xuefeng; Zheng, Tingting; Bu, Ling; Mou, Xiao; Zhou, Yuepeng; Yuan, Guoyue; Wang, Shengjun; Xiao, Yichuan

doi:10.1016/j.jaut.2016.07.008

Cited by 60 publications

(41 citation statements)

References 36 publications

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“…Increasing evidence indicates the importance of autophagy in the pathogenesis and development of inflammation [58,59]. Previous work from our laboratory has found that the LC3B-II protein expression in TFC was sharply decreased in HT tissues compared with that of the healthy controls [23,24]. In this study, LC3B-II expression in TFC was significantly decreased following treatment with IL-1β and IFN-γ, suggesting that autophagy activity in TFC was suppressed under a Th1 cytokines environment.…”

Section: Discussionsupporting

confidence: 52%

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Caveolin-1 regulates autophagy activity in thyroid follicular cells and is involved in Hashimoto’s thyroiditis disease

Luo

Mao

et al. 2018

Endocr J

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Hashimoto's thyroiditis (HT) is considered a T helper-type 1 (Th1) cytokine-dominant autoimmune thyroid disease. Caveolin-1 (Cav-1), a part of the thyroxisome multiprotein complex, is localized at the apical pole of thyrocytes and is indispensable for synthesis of thyroid hormones and modulation of oxidative stress in order to avoid cell damage and apoptosis. Reduced autophagy induces thyroid follicular cells (TFC) apoptosis by activating reactive oxygen species (ROS) in HT patients. Nevertheless, whether Cav-1 has roles in the regulation of autophagy remains largely unclear. In this study, we examined Th1 cytokines and Cav-1 expression in HT thyroid tissues, determined the effects of interleukin-1beta (IL-1β) and interferon-gamma (IFN-γ) on Cav-1 and autophagy activity in TFC, and investigated the association between Cav-1 and autophagy activity in vitro. Our results indicate that higher levels of IL-1β and IFN-γ and lower levels of Cav-1 were expressed in thyroid tissues of HT patients than in those of normal controls. Cav-1 mRNA and protein levels were significantly decreased in TFC exposed to IL-1β and IFN-γ, accompanied by decreased expression of autophagy-related protein LC3B-II. Interestingly, small interfering RNA (siRNA)-mediated Cav-1 knockdown in TFC reduced LC3B-II protein expression. Taken together, these results suggest that lack of Cav-1 expression inhibited autophagy activity in TFC exposed to Th1 cytokines (IL-1β and IFN-γ), which might be a novel pathogenetic mechanism of HT.

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Section: Discussionsupporting

confidence: 52%

“…Inhibition of autophagy may contribute to a bioenergetic shortage and favour oxidative reactions that trigger cell death characterized by hallmarks of apoptosis [22]. Autophagy activity is decreased and apoptosis level is increased in HT thyroids compared to in control thyroids [23,24]. Cav-1 has been associated with the apoptosis of thyroid cells [18].…”

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confidence: 99%

Caveolin-1 regulates autophagy activity in thyroid follicular cells and is involved in Hashimoto’s thyroiditis disease

Luo

Mao

et al. 2018

Endocr J

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“…These results indicated that excessive iodide exposure may cause nervous system impairment and ultimately induce intellectual damage, which was consistent with Zhao's study . Additionally, the concentrations used in our study were chosen based on the cytotoxic effects derived from the CCK‐8 trial, which were largely consistent with other reports investigating the toxic effects of excessive iodine on human thyroid cells …”

Section: Discussionmentioning

confidence: 87%

Oxidative stress‐mediated autophagic cell death participates in the neurotoxic effect on SH‐SY5Y cells induced by excessive iodide

Liu

Wang

Zeng

et al. 2018

Environmental Toxicology

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Excessive iodide could induce intellectual damage in children, which has attracted broad attention. To investigate the neurotoxic effect of iodide and its mechanism, a human dopaminergic neuroblastoma cell line (SH-SY5Y) was treated with different concentrations of potassium iodide (KI). The results showed that excessive iodide could decrease cell viability, reduce glutathione (GSH) and superoxide dismutase (SOD), and increase the degree of autophagy (by changing the cellular ultrastructure and raising the autophagy-related mRNA and protein expression of LC3, Beclin1, and p62), which were correlated with the immunofluorescence labeling. Furthermore, treatment with the autophagy inhibitor 3-methyladenine (3MA), antioxidant N-acetylcysteine (NAC) and 30 mM KI for 24 h was conducted in the following research. 3MA significantly decreased autophagy-related mRNA and protein expression and improved cell viability, indicating that excess iodide induced autophagic cell death. In addition, oxidative stress regulated autophagy, reflected by the results that NAC decreased the mRNA and protein expression of LC3, Beclin1, and p62. In summary, autophagic cell death mediated by oxidative stress may participate in excessive iodide-induced SH-SY5Y cell death.

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“…In a meta-analysis of a series of studies, moderate iodine excess (median urinary iodine excretion > 220 μg/L) was associated with a high prevalence of hypothyroidism in elderly patients [16]. Xu et al in their research using cell culture, thyroid follicular cells with in vitro excess iodine have been shown to contribute to the suppression of autophagy activity and apoptosis [17]. In a study conducted in Northern Morocco, there was a temporary enhancement in the prevalence of > 300 0 (0) 0 (0) Note: UIC -urinary iodine concentration.…”

Section: Discussionmentioning

confidence: 99%

Чи Існує Зв’язок Між Хворобою Хашимото І Рівнем Йоду В Сечі?

Turgut¹,

Erdoğan²,

Yürekli³

et al. 2021

Mìžnarodnij endokrinologìčnij žurnal

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Background. Hashimoto's thyroiditis (HT) is an autoimmune disease which genetic and environmental factors play a role. One of the environmental risk factors is dietary iodine intake. Urinary iodine excretion in balanced diet is equally acceptable with received iodine. It's thought that high urinary iodine excretion was associated with autoimmune thyroid diseases. We purposed to investigate whether urinary iodine level is higher in patients with HT than population. Materials and methods. 64 new patients with HT and 39 healthy volunteers were included. Age, gender, serum free-triiodothyronine (fT 3), free-thyroxine (fT 4), thyroid-stimulating hormone (TSH), anti thyroid peroxidase antibody (anti-TPO), anti thyroglobulin antibody (anti-TG) and urinary iodine concentration (UIC) were evaluated. Thyroid ultrasonography was performed. UIC were measured by Sandell-Kolthoff method. Results. There was no significant relationship was found between total thyroid volume and UIC in our study (p > 0.05). There was no significant difference between the fT 3 , fT 4 , anti-TPO, anti-TG and thyroid volume values of the individuals with urinary iodine levels below and above 100 μg/L. The difference between two subgroups was found to be significant only when TSH values were compared (p = 0.04). There was no significant difference between total thyroid volumes. No relation was found between HT and urine iodine levels in our study. The fact that the prevalence of HT in our country is similar to the literature makes us question the role of dietary iodine in the etiology. Conclusions. At the iodine-deficient regions such as our country relationship between urinary iodine excretion and HT needs to be investigated.

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

Cited by 60 publications

References 36 publications

Caveolin-1 regulates autophagy activity in thyroid follicular cells and is involved in Hashimoto’s thyroiditis disease

Caveolin-1 regulates autophagy activity in thyroid follicular cells and is involved in Hashimoto’s thyroiditis disease

Oxidative stress‐mediated autophagic cell death participates in the neurotoxic effect on SH‐SY5Y cells induced by excessive iodide

Чи Існує Зв’язок Між Хворобою Хашимото І Рівнем Йоду В Сечі?

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