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Prepublished online as a Blood First Edition Paper on May 1, 2003; DOI 10.1182/blood-2003-02-0347. This Article Full Text (PDF) All Versions of this Article: 2003-02-0347v1 102/5/1893    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Chen, H. Articles by Vulpe, C. D Search for Related Content PubMed PubMed Citation Articles by Chen, H. Articles by Vulpe, C. D Social Bookmarking                   What's this? Submitted February 4, 2003 Accepted April 15, 2003 Systemic regulation of HEPHAESTIN and IREG1 revealed in studies of genetic and nutritional iron deficiency Huijun Chen, Trent Su, Zouhair K Attieh, Tama C Fox, Andrew T McKie, Gregory J Anderson, and Chris D Vulpe* Department of Nutritional Sciences and Toxicology, University of California, Berkeley, CA, USA Department of Molecular Medicine, King's College, London, United Kingdom Joint Clinical Sciences Program, The Queensland Institute of Medical Research and the University of Queensland, Brisbane, QLD, Australia * Corresponding author; email: vulpe{at}uclink4.berkeley.edu. HEPHAESTIN is a membrane-bound multi-copper ferroxidase necessary for iron egress from intestinal enterocytes into the circulation. Mice with sex linked anemia (sla) have a mutant form of HEPHAESTIN and a defect in intestinal basolateral iron transport which results in iron deficiency and anemia. IREG1 (SLC11A3, also known as ferroportin1 or MTP1) is the putative intestinal basolateral iron transporter. We compared iron levels and expression of genes involved in iron uptake and storage in sla mice and C57BL/6J mice fed iron deficient, overload or control diets. Both iron deficient wild-type mice and sla mice showed increased expression of Heph and Ireg1 mRNA,compared to controls, whereas only iron deficient wild-type mice had increased expression of the brush border transporter Dmt1. Unlike iron deficient mice, sla mouse enterocytes accumulated non-heme iron and ferritin. These results indicate that DMT1 can be modulated by the enterocyte iron level, whereas HEPHAESTIN and IREG1 expression respond to systemic rather than local signals of iron status. Thus the basolateral transport step appears to be the primary site at which the small intestine responds to alterations in body iron requirements. 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