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.
Excess iodide-induced reactive oxygen species elicit iodide efflux via β-tubulin-associated ClC-3 in thyrocytes
Meisheng Yu, Yuan Wei, Pengyuan Wang, Zhiqin Deng, Jianwen Mao, Linyan Zhu, Lixin Chen, Shuang Peng, Liwei Wang; Excess iodide-induced reactive oxygen species elicit iodide efflux via β-tubulin-associated ClC-3 in thyrocytes. Biochem J 18 March 2022; 479 (5): 629–640. doi: https://doi.org/10.1042/BCJ20210709
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