Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the effect of iron on the expression of transferrin receptors (TrfRs) and ferritin chains in cultures of human peripheral blood monocytes maturing to macrophages. Monocyte-macrophage maturation is associated with a gradual rise of Trf-binding capacity in the absence of cell proliferation. At all culture times, treatment with ferric ammonium citrate induces a dose-dependent rise of the Trf-binding level as compared with nontreated cells. Scatchard analysis revealed that this phenomenon is due to an increase in receptor number rather than an alteration in ligand-receptor affinity. Biosynthesis experiments indicated that the rise in number of TrfRs is due to an increase of receptor synthesis, which is associated with a sustained elevation of the TrfR RNA level. The up-regulation of TrfR synthesis is specific in that expression of other macrophage membrane proteins is not affected by iron addition. Conversely, addition of an iron chelator induced a slight decrease of TrfR synthesis. The expression of heavy and light ferritin chains at RNA and protein levels was markedly more elevated in cultured macrophages than in fresh monocytes, thus suggesting modulation of ferritin genes at transcriptional or post-transcriptional levels. Addition of iron salts to monocyte-macrophage cultures sharply stimulated ferritin synthesis but only slightly enhanced the level of ferritin RNA, thus indicating a modulation at the translational level. These results suggests that in cultured human monocytes-macrophages, iron up-regulates TrfR expression, thus in sharp contrast to the negative feedback reported in a variety of other cell types. These observations may shed light on the mechanism(s) of iron storage in tissue macrophages under normal conditions and possibly on the pathogenesis of diseases characterized by abnormal iron storage.
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PMID:Iron up-modulates the expression of transferrin receptors during monocyte-macrophage maturation. 247 88

The national and international recommendations concerning the iron management in chronic kidney disease (CKD) patient are well established. All acknowledge the fact that iron needs are increased in uremic patients. This is particularly true for CKD-5 patients treated by hemodialysis (increased losses) and when treated by an erythropoetic stimulating agent (ESA). Annual iron requirements are currently estimated between 500 mg and 3000 mg per year. The biodisponibility of oral iron isreduced and side effects are quite common. The venous supplementation of iron offers today the best safety/efficacy profile. The evaluation of iron store is mandatory in CKD patient. The assessment of iron store in kidney patient relies on three major markers: transferrin saturation (Trf Sat); ferritin; percentage of hypochromic erythroid cells. Faced to iron deficiency, it is crucial to differentiate two situations: an absolute iron deficiency (Trf Sat < 20 % ; ferritin < 100 ng/ml; percentage of hypochromic cells > 10%); a functional iron deficiency (Trf Sat < 20%; ferritin > 200-500 ng/ml; percentage of hypochromic cells > 5-10%). When intravenous iron supplementation is indicated, dosing regime should be based on a slow and a reduced dosage administration to comply with manufacturer and best practice recommendations. Regular iron infusion of 50 to 100 mg per week is able to cover the basic needs for most hemodialysis patients.
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PMID:[Recommendations of iron management in chronic kidney patients]. 1737 84

Diabetes mellitus is associated with altered iron homeostasis that can potentially effect reactive oxygen species generation and contribute to diabetes-related complications. We investigated, by quantitative polymerase chain reaction, whether the expression of liver hepcidin, ferritin, and TfR-1 is altered in diabetes. Rats in the control (C) group received a standard diet; control iron (CI) group received a standard diet supplemented with iron; diabetic (D) group received an injection of streptozotocin; and diabetic iron (DI) group received streptozotocin and the diet with iron. Animals of the D group showed higher levels of serum iron, increased concentration of carbonyl protein, and a decrease in antioxidant status. Group D rats showed increased hepatic expression of Trf-1 compared to the other groups. Iron supplementation reversed this increase. Hepcidin mRNA was 81% higher in DI than in C and CI rats. The results suggest that diabetes, with or without excess iron, can cause perturbations in iron status, hepcidin and Trf-1 expression.
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PMID:Differential expression of iron metabolism proteins in diabetic and diabetic iron-supplemented rat liver. 2217 Jul 71