Corrigendum for Aydemir TB et al., volume 318, 2020, p. G673–G681

Aydemir TB, Thorn TL, Ruggiero CH, Pompilus M, Febo M, Cousins RJ. Intestine-specific deletion of metal transporter Zip14 (Slc39a14) causes brain manganese overload and locomotor defects of manganism. Am J Physiol Gastrointest Liver Physiol 318: G673–G681, 2020. First published March 20, 2020; doi:10.1152/ajpgi.00301.2019. In the original article “Intestine-specific deletion of metal transporter Zip14 (Slc39a14) causes brain manganese overload and locomotor defects of manganism,” a reference [Scheiber IF, Wu Y, Morgan SE, Zhao N. The intestinal metal transporter ZIP14 maintains systemic manganese homeostasis. J Biol Chem 294: 9147–9160, 2019] was not cited. The citation should have been inserted in the discussion, paragraph 3, and should have read as the following:

“The early studies with ⁵⁴Mn revealed that hepatobiliary system was a major route for Mn elimination from the body (5). However, using liver-specific Zip14-KO mice, Xin et al. (37) showed that there was no Mn accumulation in the brain or other tissues of liver-specific Zip14-KO mice, which have considerably lower hepatic Mn levels. This finding supports our hypothesis that there are other highly efficient Mn elimination routes in the body. We previously showed that ZIP14 is localized at the basolateral site of the enterocytes (3, 14). Furthermore, intestinal Mn elimination was impaired in WB Zip14-KO mice. Therefore, we generated I-KO mice to explore the specific role of intestinal Zip14 in Mn elimination/detoxification. We found that Mn transport in the serosal-to-mucosal direction was impaired and, importantly, that Mn accumulated in the blood and brain at steady state. This novel finding suggests that deletion of intestinal Zip14 is sufficient to cause systemic Mn overload and that intestinal ZIP14 is a significant contributor to Mn homeostasis (32a). Our recent results with intestine-specific Zip14-KO murine model and previous findings with whole body Zip14-KO mice (13, 14) are supported by the study where impaired basolateral-to-apical manganese transport in CaCo-2 cells and Mn changes in tissues of intestine-specific Zip14-KO mice was shown (38).”