Excess iodide-induced reactive oxygen species elicit iodide efflux via β-tubulin-associated CIC-3 in thyrocytes

作者：Yu, Meisheng; Wei, Yuan; Wang, Pengyuan; Deng, Zhiqin; Mao, Jianwen; Zhu, Linyan; Chen, Lixin^*; Peng, Shuang^*; Wang, Liwei^*

来源：Biochemical Journal, 2022, 479(5): 629-640.

DOI：10.1042/BCJ20210709

• SODIUM/IODIDE SYMPORTER
• CELLS
• CLC-3
• EXPRESSION
• TRANSPORT
• MECHANISMS
• CHANNELS
• PENDRIN
• LINE

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 (CIC-3) involvement in the iodide (I-) efflux from thyrocytes remains unclear. Therefore, we examined the effects of CIC-3 on I- efflux. CIC-3 expression was found to significantly alter the serum TT3 and TT4 concentrations in mice. We further found that excess I- stimulation affected CIC-3 expression, distribution, and I- efflux in FRTL-5 cells. Immunofluorescence analyses indicated that CIC-3 mainly accumulated in the cell membrane and co-localized with beta-tubulins after 24 h of excess I- treatment, and that this process depended on ROS production. Thus, CIC-3 may be involved in I- efflux at the apical pole of thyrocytes via excess I--induced ROS production and beta-tubulin polymerization. Our results reveal novel insights into the role of CIC-3 in I- transport and thyroid function.

• 单位
  1; 广东药学院