Decreased hephaestin expression and activity leads to decreased iron efflux from differentiated Caco2 cells

Journal of Cellular Biochemistry - Tập 107 Số 4 - Trang 803-808 - 2009
Huijun Chen1,2, Zouhair K. Attieh3,1, Thi Dang1, Gang Huang1, R. M. van der Hee1,4, Chris D. Vulpe1
1Department of Nutritional Science and Toxicology, University of California, Berkeley, California 94720-3104
2Medical School, Nanjing University, Nanjing, China
3Department of Clinical Laboratory Science, American University of Science and Technology, Ashrafieh, Lebanon
4Unilever Research and Development Vlaardingen, Vlaardingen, The Netherlands

Tóm tắt

AbstractIron 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, ferroportin1, and hephaestin, a ferroxidase. Copper deficiency leads to reduced hephaestin protein expression and activity in mouse enterocytes and intestinal cell lines. We tested the effect of copper deficiency on differentiated Caco2 cells grown in transwells and found decreased hephaestin protein expression and activity as well as reduced ferroportin1 protein levels. Furthermore, the decrease in hephaestin levels 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. J. Cell. Biochem. 107: 803–808, 2009. © 2009 Wiley‐Liss, Inc.

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Thông tin xuất bản

Journal of Cellular Biochemistry

Tập 107 Số 4

803-808

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