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- Title
Disruption of the mouse <italic>Slc39a14</italic> gene encoding zinc transporter ZIP14 is associated with decreased bone mass, likely caused by enhanced bone resorption.
- Authors
Sasaki, Sun; Tsukamoto, Manami; Saito, Masaki; Hojyo, Shintaro; Fukada, Toshiyuki; Takami, Masamichi; Furuichi, Tatsuya
- Abstract
Osteoclasts are bone‐resorbing cells that play an essential role in maintaining bone homeostasis. Zinc (Zn) has been reported to inhibit osteoclast‐mediated bone resorption, but the mechanism of this action has not been clarified. Zn homeostasis is tightly controlled by the coordinated actions of many Zn transporters. The Zn transporter ZIP14/Slc39a14 is involved in various physiological functions; hence, <italic>Zip14</italic>‐knockout (KO) mice exhibit multiple phenotypes. In this study, we thoroughly investigated the bone phenotypes of <italic>Zip14</italic>‐KO mice, demonstrating that the KO mice exhibited osteopenia in both trabecular and cortical bones. In <italic>Zip14</italic>‐KO mice, bone resorption was increased, whereas the bone formation rate was unchanged. <italic>Zip14</italic>mRNA was expressed in normal osteoclasts both <italic>in vivo</italic> and <italic>in vitro</italic>, but receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis was not impaired in bone marrow‐derived macrophages prepared from <italic>Zip14</italic>‐KO mice. These results suggest that ZIP14 regulates bone homeostasis by inhibiting bore resorption and that in <italic>Zip14</italic>‐KO mice, bone resorption is increased due to the elimination of this inhibitory regulation. Further studies are necessary to conclude whether the enhancement of bone resorption in <italic>Zip14</italic>‐KO mice is due to a cell‐autonomous or a non‐cell‐autonomous osteoclast defect.
- Subjects
ZINC transporters; BONE resorption; OSTEOCLASTS; HOMEOSTASIS; OSTEOPENIA; LABORATORY mice
- Publication
FEBS Open Bio, 2018, Vol 8, Issue 4, p655
- ISSN
2211-5463
- Publication type
Article
- DOI
10.1002/2211-5463.12399