The iodide transporter Slc26a7 impacts thyroid function more strongly than Slc26a4 in mice

Naoya Yamaguchi, Atsushi Suzuki, Aya Yoshida, Tatsushi Tanaka, Kohei Aoyama, Hisashi Oishi, Yuichiro Hara, Tomoo Ogi, Izuki Amano, Satomi Kameo, Noriyuki Koibuchi, Yasuhiro Shibata, Shinya Ugawa, Haruo Mizuno, Shinji Saitoh

Research output: Contribution to journalArticlepeer-review

Abstract

SLC26A4 is a known iodide transporter, and is localized at the apical membrane of thyrocytes. Previously, we reported that SLC26A7 is also involved in iodide transport and that Slc26a7 is a novel causative gene for congenital hypothyroidism. However, its detailed role in vivo remains to be elucidated. We generated mice that were deficient in Slc26a7 and Slc26a4 to delineate differences and associations in their roles in iodide transport. Slc26a7−/− mice showed goitrous congenital hypothyroidism and mild growth failure on a normal diet. Slc26a7−/− mice with a low iodine environment showed marked growth failure. In contrast, Slc26a4−/− mice showed no growth failure and hypothyroidism in the same low iodine environment. Double-deficient mice showed more severe growth failure than Slc26a7−/− mice. RNA-seq analysis revealed that the number of differentially expressed genes (DEGs) in Slc26a7−/− mice was significantly higher than that in Slc26a4−/− mice. These indicate that SLC26A7 is more strongly involved in iodide transport and the maintenance of thyroid function than SLC26A4.

Original languageEnglish
Article number11259
JournalScientific reports
Volume12
Issue number1
DOIs
Publication statusPublished - 12-2022

All Science Journal Classification (ASJC) codes

  • General

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