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Excess iodide-induced reactive oxygen species elicit iodide efflux via β-tubulin-associated ClC-3 in thyrocytes
Biochemical Journal ( IF 4.1 ) Pub Date : 2022-03-18 , DOI: 10.1042/bcj20210709
Meisheng Yu 1 , Yuan Wei 2 , Pengyuan Wang 1 , Zhiqin Deng 3 , Jianwen Mao 4 , Linyan Zhu 1 , Lixin Chen 5 , Shuang Peng 1 , Liwei Wang 1
Affiliation  

Iodide (I−) is crucial to thyroid function, and its regulation in thyrocytes involves ion transporters and reactive oxygen species (ROS). However, the extent of 2Cl−/H+ exchanger (ClC-3) involvement in the iodide (I−) efflux from thyrocytes remains unclear. Therefore, we examined the effects of ClC-3 on I− efflux. ClC-3 expression was found to significantly alter the serum TT3 and TT4 concentrations in mice. We further found that excess I− stimulation affected ClC-3 expression, distribution, and I− efflux in FRTL-5 cells. Immunofluorescence analyses indicated that ClC-3 mainly accumulated in the cell membrane and co-localized with β-tubulins after 24 h of excess I− treatment, and that this process depended on ROS production. Thus, ClC-3 may be involved in I− efflux at the apical pole of thyrocytes via excess I−-induced ROS production and β-tubulin polymerization. Our results reveal novel insights into the role of ClC-3 in I− transport and thyroid function.

中文翻译:

过量的碘化物诱导的活性氧通过甲状腺细胞中的 β-微管蛋白相关的 ClC-3 引起碘化物流出

碘化物 (I-) 对甲状腺功能至关重要,其在甲状腺细胞中的调节涉及离子转运蛋白和活性氧 (ROS)。然而,2Cl-/H+ 交换剂 (ClC-3) 参与碘化物 (I-) 从甲状腺细胞流出的程度仍不清楚。因此,我们检查了 ClC-3 对 I- 流出的影响。发现 ClC-3 表达显着改变小鼠血清 TT3 和 TT4 浓度。我们进一步发现,过量的 I- 刺激会影响 FRTL-5 细胞中 ClC-3 的表达、分布和 I- 流出。免疫荧光分析表明,在过量 I- 处理 24 小时后,ClC-3 主要在细胞膜中积累并与 β-微管蛋白共定位,并且该过程取决于 ROS 的产生。因此,ClC-3 可能通过过量的 I- 诱导的 ROS 产生和 β-微管蛋白聚合参与甲状腺细胞顶端的 I- 流出。我们的结果揭示了对 ClC-3 在 I- 转运和甲状腺功能中的作用的新见解。
更新日期:2022-03-04
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