Hepcidin inhibits apical iron uptake in intestinal cells
Author
dc.contributor.author
Mena, Natalia P.
Author
dc.contributor.author
Esparza, Andrés
Author
dc.contributor.author
Tapia, Victoria
Author
dc.contributor.author
Valdés, Pamela
Author
dc.contributor.author
Núñez González, Marco
Admission date
dc.date.accessioned
2018-12-20T15:10:00Z
Available date
dc.date.available
2018-12-20T15:10:00Z
Publication date
dc.date.issued
2007
Cita de ítem
dc.identifier.citation
American Journal of Physiology - Gastrointestinal and Liver Physiology, Volumen 294, Issue 1, 2018,
Identifier
dc.identifier.issn
01931857
Identifier
dc.identifier.issn
15221547
Identifier
dc.identifier.other
10.1152/ajpgi.00122.2007
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/158102
Abstract
dc.description.abstract
Hepcidin (Hepc) is considered a key mediator in iron trafficking. Although the mechanism of Hepc action in macrophages is fairly well established, much less is known about its action in intestinal cells, one of the main targets of Hepc. The current study investigated the effects of physiologically generated Hepc on iron transport in Caco-2 cell monolayers and rat duodenal segments compared with the effects on the J774 macrophage cell line. Addition of Hepc to Caco-2 cells or rat duodenal segments strongly inhibited apical 55Fe uptake without apparent effects on the transfer of 55Fe from the cells to the basolateral medium. Concurrently, the levels of divalent metal transporter 1 (DMT1) mRNA and protein in Caco-2 cells decreased while the mRNA and protein levels of the iron export transporter ferroportin did not change. Plasma membrane localization of ferroportin was studied by selective biotinylation of apical and basolateral membrane domains; Hepc induced rapid internalization of ferr