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Decreased hephaestin expression and activity leads to decreased iron efflux from differentiated Caco2 cells
Author(s) -
Vulpe Chris,
Attieh Zouhair K,
Chen Huijun
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.304.3
Subject(s) - ceruloplasmin , enterocyte , transferrin , ferroportin , chemistry , caco 2 , transferrin receptor , dmt1 , microbiology and biotechnology , transporter , medicine , endocrinology , cell , biochemistry , small intestine , iron homeostasis , biology , metabolism , gene
Iron is transported across intestinal brush border cells into the circulation in at least two distinct steps. Iron can enter the enterocyte via the apical surface through several paths. However, iron egress from the basolateral side of enterocytes converges on a single export pathway requiring the iron transporter, ferroportin, and hephaestin, a ferroxidase. Copper deprivation leads to reduced hephaestin protein expression and activity in mouse enterocytes and intestinal cell lines. We tested the effect of copper deprivation in differentiated Caco2 cells grown in transwells and found decreased hephaestin protein expression and activity. Furthermore, this decrease correlates with a decrease of 55Fe release from the basolateral side of Caco2 cells. Presence of ceruloplasmin, apo‐transferrin or holo‐transferrin did not significantly alter the results observed. Repletion of copper in Caco2 cells leads to reconstitution of Hephaestin protein expression, activity and transepithelial iron transport.