The role of NO in macrophage iron turnover was studied in macrophages from inducible nitric oxide synthase (iNOS)-deficient mice. Interferon γ/lipopolysaccharide (IFNγ/LPS)-activated bone marrow-derived macrophages from iNOS-deficient mice, following phagocytosis of 59Fe-labelled transferrin—anti-transferrin immune complexes, showed reduced iron release compared with cells from wild-type iNOS littermates. Uptake of the complexes by macrophages was similar in iNOS-deficient and wild-type mice. Ferritin was up-regulated by IFNγ/LPS treatment, but NO exercised a modest opposing down-regulatory effect. No effect of iNOS deficiency was seen when iron was taken up from iron citrate, which enters via a non-phagocytic route. These results suggest that NO plays a key role in regulating iron turnover in macrophages acquiring iron by phagocytosis of erythrocytes or cell debris, and thus the supply to peripheral tissues, such as to the bone marrow for erythropoiesis.
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Research Article| July 01 2002
Regulation of phagosomal iron release from murine macrophages by nitric oxide
Victoriano MULERO 1
∗Department of Immunology and Bacteriology, Western Infirmary, University of Glasgow, Glasgow, U.K.
†Department of Cell Biology, Faculty of Biology, University of Murcia, 30100 Murcia, Spain
1To whom correspondence should be addressed, at the Department of Cell Biology, Faculty of Biology, University of Murcia, 30100 Murcia, Spain (e-mail email@example.com).
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Victoriano MULERO, Xiao-qing WEI, Foo Y. LIEW, Jeremy H. BROCK; Regulation of phagosomal iron release from murine macrophages by nitric oxide. Biochem J 1 July 2002; 365 (1): 127–132. doi: https://doi.org/10.1042/bj20011875
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