1. Academic Validation
  2. The iodide transporter Slc26a7 impacts thyroid function more strongly than Slc26a4 in mice

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

  • Sci Rep. 2022 Jul 4;12(1):11259. doi: 10.1038/s41598-022-15151-4.
Naoya Yamaguchi  # 1 Atsushi Suzuki  # 1 Aya Yoshida 1 Tatsushi Tanaka 2 Kohei Aoyama 3 Hisashi Oishi 4 Yuichiro Hara 5 6 Tomoo Ogi 5 6 Izuki Amano 7 Satomi Kameo 8 Noriyuki Koibuchi 7 Yasuhiro Shibata 9 Shinya Ugawa 9 Haruo Mizuno 10 Shinji Saitoh 1
Affiliations

Affiliations

  • 1 Department of Pediatrics and Neonatology, Nagoya City University Graduate School of Medical Sciences, 1-Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, 467-8601, Japan.
  • 2 Department of Pediatrics, Toyohashi Municipal Hospital, Toyohashi, Japan.
  • 3 Department of Pediatrics and Neonatology, Nagoya City University Graduate School of Medical Sciences, 1-Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, 467-8601, Japan. [email protected].
  • 4 Department of Comparative and Experimental Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
  • 5 Department of Genetics, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.
  • 6 Department of Human Genetics and Molecular Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
  • 7 Department of Integrative Physiology, Gunma University Graduate School of Medicine, Maebashi, Japan.
  • 8 Department of Nutrition, Koshien University, Takarazuka, Japan.
  • 9 Department of Anatomy and Neuroscience, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
  • 10 Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Japan.
  • # Contributed equally.
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.

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