Open AccessExcess iodide-induced reactive oxygen species elicit iodide efflux via β-tubulin-associated ClC-3 in thyrocytes
Author(s) -
Meisheng Yu,
Wei Yuan,
Pengyuan Wang,
Zhiqin Deng,
Jianwen Mao,
Linyan Zhu,
Lixin Chen,
Shuang Peng,
Liwei Wang
Publication year - 2022
Publication title -
biochemical journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.706
H-Index - 265
eISSN - 1470-8728
pISSN - 0264-6021
DOI - 10.1042/bcj20210709
Subject(s) - efflux , iodide , reactive oxygen species , chemistry , intracellular , stimulation , microbiology and biotechnology , tubulin , biophysics , biochemistry , microtubule , biology , endocrinology , organic chemistry
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.