Artículos de revistas
Hepcidin inhibits apical iron uptake in intestinal cells
Fecha
2007Registro en:
American Journal of Physiology - Gastrointestinal and Liver Physiology, Volumen 294, Issue 1, 2018,
01931857
15221547
10.1152/ajpgi.00122.2007
Autor
Mena, Natalia P.
Esparza, Andrés
Tapia, Victoria
Valdés, Pamela
Núñez González, Marco
Institución
Resumen
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