PMID: 11925462Apr 2, 2002Paper

Iron treatment downregulates DMT1 and IREG1 mRNA expression in Caco-2 cells

The Journal of Nutrition
Ligia A MartiniRichard J Wood

Abstract

Iron deficiency is the most common nutritional disorder worldwide, whereas pathologic elevations of body iron stores can occur under certain circumstances due to genetic abnormalities or in association with other diseases. The intestine is the exclusive locus of homeostatic regulation of body iron stores, which is accomplished by changes in iron absorption efficiency by largely unknown molecular mechanisms in response to alterations in body iron stores. Recently, a number of novel genes involved in iron metabolism, such as the iron uptake transporter DMT1/DCT1/Nramp2 and the iron export transporter IREG1/ferroportin1/MTP1, have been identified, providing important insights about molecular aspects of intestinal iron absorption and its regulation. The aim of this study was to investigate the effects of iron treatment on DMT1 and IREG1 mRNA expression in Caco-2 cells, a human intestinal cell line. Exposure of the cells to iron (200 micromol/L ferric nitrilotriacetic acid for 72 h) significantly decreased transferrin receptor mRNA (80%), DMT1 mRNA (57%) and IREG1 mRNA (52%). These observations are consistent with the notion of parallel regulation of these iron-responsive genes in vivo to protect the enterocyte from iron toxicity an...Continue Reading

References

Nov 18, 1991·Biochimica Et Biophysica Acta·X Alvarez-HernandezJ Glass
Aug 6, 1996·Proceedings of the National Academy of Sciences of the United States of America·M W Hentze, L C Kühn
Aug 1, 1997·Nature Genetics·J V Gray, K J Johnson
Aug 1, 1997·The American Journal of Clinical Nutrition·L HallbergE Gramatkovski
Dec 31, 1997·The Journal of Cell Biology·J A GutierrezM Wessling-Resnick
Nov 10, 1998·The Journal of Nutrition·R J Wood, O Han
Mar 17, 1999·Proceedings of the National Academy of Sciences of the United States of America·R E FlemingW S Sly
Apr 5, 2000·The Journal of Biological Chemistry·S Abboud, D J Haile
Aug 15, 2000·Annual Review of Nutrition·R S Eisenstein

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Citations

Sep 26, 2008·European Journal of Nutrition·Nathalie M Scheers, Ann-Sofie Sandberg
Jan 15, 2009·The Journal of Nutrition·Fikret AydemirMitchell D Knutson
Mar 1, 2012·Cellular and Molecular Neurobiology·Emanuela UrsoMichele Maffia
Sep 3, 2013·Expert Review of Hematology·Wei-Na KongYan-Zhong Chang
Jun 26, 2020·Metallomics : Integrated Biometal Science·Haoxuan DingJie Feng
Jan 19, 2006·The Journal of Biological Chemistry·Henry MokArmin Schumacher
Sep 10, 2010·Advances in Hematology·Luciano CianettiNadia Maria Sposi
Feb 9, 2008·American Journal of Physiology. Gastrointestinal and Liver Physiology·James F CollinsRichard W Browne
May 21, 2003·Critical Reviews in Clinical Laboratory Sciences·Jayong Chung, Marianne Wessling-Resnick
Jan 31, 2004·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Antonello Pietrangelo
Sep 25, 2014·Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society·Karan M ShahJ Mark Wilkinson
Oct 22, 2003·Journal of Hepatology·Athina LymboussakiAntonello Pietrangelo
Apr 23, 2005·Toxicology and Applied Pharmacology·Christy C Bridges, Rudolfs K Zalups
Sep 30, 2005·Journal of Agricultural and Food Chemistry·Chi Kong YeungDennis D Miller

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