Immunolocalization of Ferroportin in Healthy and Anemic Mice
María Cecilia D’Anna 1, Tania Vanesa Veuthey 1 and Marta Elena Roque 1*
1 Laboratory of Human Physiology, Department of Biology, Biochemistry and Pharmacy, Universidad Nacional del Sur, Bahía Blanca, Argentina
* To whom correspondence should be addressed. E-mail: mroque{at}uns.edu.ar.
Submitted on April 14, 2008
Accepted on 26 August 2008
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Abstract |
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Ferroportin (FPN), the only iron exporter identified to date, participates in iron release from enterocytes and macrophages, regulating its absorption and recycling. We used a murine model of experimental hemolytic anemia to study adaptive changes in the localization of FPN in duodenum, liver and spleen. FPN was assessed by immunohistochemistry in healthy and anemic mice using rabbit anti-mouse FPN polyclonal antibodies. Goat-labeled polymer-HRP anti-rabbit Envision+System(DAB) was used as secondary antibody. Tissue iron was studied by Prussian Blue iron staining. Anemia evolution and erythropoietic recovery was assessed using conventional hematological tests. Healthy mice showed mainly supranuclear expression of FPN in enterocytes and a weak basolateral expression, whereas in anemic mice the expression was detected mainly at the basolateral membrane (days 4, 5). Red pulp macrophages of healthy mice showed FPN-hemosiderin co-localization. In liver of healthy mice, FPN was mainly cytoplasmic, whereas in anemic mice it was redistributed to the cell membrane. Our findings clearly demonstrate that anemia induces adaptive changes in FPN expression, contributing to anemia restoration by increasing available iron. FPN expression in the membrane is the main pathway of iron release. Our data indicate that iron homeostasis in vivo is maintained through the coordinated expression of this iron exporter in both intestinal and phagocytic cells.
Key Words:
ferroportin, anemia, iron, enterocytes, macrophages
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