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)

The effects of recombinant murine macrophage inflammatory protein (MIP)-1 beta and MIP-2 on the suppressive activity of MIP-1 alpha were tested using colony formation by human and murine bone marrow burst-forming unit-erythroid (BFU-E), colony-forming unit-granulocyte erythroid macrophage, megakaryocyte (CFU-GEMM), and colony-forming unit-granulocyte macrophage (CFU-GM) progenitor cells. MIP-1 beta, but not MIP-2, when added with MIP-1 alpha to cells, blocked the suppressive effects of MIP-1 alpha on both human and murine BFU-E, CFU-GEMM, and CFU-GM colony formation. Similar results were observed regardless of the early acting cytokines used: human rGM-CSF plus human rIL-3, and two recently described potent cytokines, a genetically engineered human rGM-CSF/IL-3 fusion protein and MGF, a c-kit ligand. The more potent the stimuli, the greater the suppressive activity noted. Pulse treatment of hu bone marrow cells with MIP-1 alpha at 4 degrees C for 1 h was as effective in inhibiting colony formation as continuous exposure of cells to MIP-1 alpha, and the pulsing effect with MIP-1 alpha could not be overcome by subsequent exposure of cells to MIP-1 beta. Also, pulse exposure of cells to MIP-1 beta blocked the activity of subsequently added MIP-1 alpha. For specificity, the action of a nonrelated myelosuppressive factor H-ferritin, was compared. MIP-1 alpha and H-ferritin were shown to act on similar target populations of early BFU-E, CFU-GEMM, and CFU-GM. MIP-1 beta did not block the suppressive activity of H-ferritin. Also, hemin and an inactive recombinant human H-ferritin mutein counteracted the suppressive effects of the wildtype H-ferritin molecule, but did not block the suppressive effects of MIP-1 alpha. These results show that MIP-1 beta's ability to block the action of MIP-1 alpha is specific. In addition, the results suggest that MIP-1 alpha and MIP-beta can, through rapid action, modulate early myeloid progenitor cell proliferation.
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PMID:Macrophage inflammatory protein (MIP)-1 beta abrogates the capacity of MIP-1 alpha to suppress myeloid progenitor cell growth. 191 79

A case of peripheral T-cell lymphoma classified, according to the updated Kiel classification, as a large pleomorphic T-cell lymphoma with a high content of reactive histiocytes and blood hypereosinophilia is reported. Light microscopic examination revealed a diffuse effacement of the lymph node structure by large pleomorphic lymphoma cells mixed with eosinophils and many histiocytes, some of them presenting discrete features of hemophagocytosis. The neoplastic cells were CD3, CD5, CD8 and HLA-DR positive but failed to show CD30 antigen. DNA molecular analysis displayed simultaneous rearrangements of the genes coding for the delta chain of the T-cell receptor and for the Ig heavy chain. Increased serum levels of angiotensin converting enzyme and ferritin were found and probably induced by the reactive histiocytes. Immunoassays (ELISA) with antibodies directed against some cytokines and against the Tac peptide (sIL-2R) were performed. They demonstrated high serum levels of sIL-2R and a slight increase in GM-CSF, but neither IL-5 nor IL-3. The association of blood hypereosinophilia and histiocytic hyperplasia with a peripheral T-cell lymphoma is discussed.
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PMID:A case of pleomorphic T-cell lymphoma with a high content of reactive histiocytes presented with hypereosinophilia. 747 65

A number of cytokines have been implicated in the suppression of myeloid stem and progenitor cell proliferation. It has been suggested that some of these act directly on the stem/progenitors themselves, based on the effects of these cells, plated in culture at low seeding densities, on highly enriched populations. These studies, however, do not definitively rule out effects on accessory cells. To more rigorously evaluate direct-acting suppressive effects of cytokines, such cytokines were assessed for their effects on colony formation initiated by single bone marrow (BM) or umbilical cord blood (CB) CD34 cells sorted into single wells in the presence of a combination of growth-stimulating cytokines (erythropoietin [Epo], steel factor [SLF], granulocyte-macrophage colony-stimulating factor [GM-CSF], and interleukin-3 [IL-3]) and in the presence or absence of serum. Under these conditions, it was demonstrated that H-ferritin, transforming growth factor-beta 1 (TGF-beta 1), and members of the chemokine family (macrophage inflammatory protein-1 alpha [MIP-1 alpha], MIP-2 beta, platelet factor 4 [PF4], IL-8, and macrophage chemotactic and activating factor [MCAF]) had direct significant suppressive activities on single stem/progenitor cells from adult human BM in the presence or absence of serum. Single sorted CB cells were much less sensitive to inhibition by these cytokines. The reasons for this differential sensitivity are not known. Of possible relevance to this for cytokines, such as H-ferritin and the chemokines that have actions during S-phase of the cell cycle, CB progenitors were in slower cycle at initiation of culture than were BM progenitors.
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PMID:Comparative effects of suppressive cytokines on isolated single CD34(3+) stem/progenitor cells from human bone marrow and umbilical cord blood plated with and without serum. 769 34

A variety of hematopoietic factors including granulocyte macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), interleukin 3 (IL-3) and thrombopoietin (TPO) induce a rapid increase of intracellular reactive oxygen species (ROS). ROS induces the activation of many signaling molecules, including Shc, Lck, syk, PKC, MAPK, STAT3, through inhibition of protein phosphatase. Each growth factor has a specific cell-surface receptor, which activates both unique and shared signal transduction pathways. The processes of signal transduction linking cell-surface receptor to the formation of intracellular ROS have not been elucidated fully. Ferritins are composed of two subunit types, H and L, and made of 24 subunits that sequester up to 4500 atoms of iron. When the stored iron atoms are released from H-ferritin, through iron-catalyzed reaction, they have the capacity to promote the formation of ROS. Here, the interaction of G-CSFR and H-ferritin was confirmed by yeast two-hybrid screen, mammalian two-hybrid assays, glutathione-S-transferase (GST) pull-down experiments and immunoprecipitation studies in vitro and in vivo. Additional immunofluorescence assay showed that the two proteins colocalized along the plasma membrane and partly in the cytoplasm. The binding site for H-ferritin was demonstrated to locate to the box3 motif on the C-terminal region of granulocyte colony-stimulating factor receptor (G-CSFR). Furthermore, we found the interaction of full-length G-CSFR with H-ferritin was dissociated at 30 minutes after G-CSF induction and then began to assemble at 45 minutes. The labile iron pool (LIP) is a pool of redox-active iron complexes, which is regulated tightly by the expression of H-ferritin. Experiments showed that the level of LIP increased significantly at 30 minutes after G-CSF stimulation and intracellular ROS formation changed in a pattern similar to LIP response to G-CSF in bone-marrow hematopoietic cells. G-CSF-induced changes in the level of LIP and ROS formation could be blocked by pretreatment with iron chelators that repressed the expression of H-ferritin. In addition, the phosphorylation of STAT3 induced by G-CSF was decreased in iron chelator-treated hematopoietic cells. These data suggested that LIP may be released from the dissociated H-ferritin, and then induce intracellular ROS formation in the bone-marrow hematopoietic cells. ROS, acting as a second messenger, might take part in G-CSF receptor signal transduction. So, here, a new G-CSFR-H-ferritin-LIP-ROS pathway is proposed for regulation of intracellular ROS formation in bone-marrow hematopoietic cells.
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PMID:Regulation of LIP level and ROS formation through interaction of H-ferritin with G-CSF receptor. 1512 26

In Georgia, we were first who tried to study adolescent pregnant women with anemia (age group 14-18ys). We studied the reasons which have caused anemia in the pregnant women of this age. This gave us the opportunity to chose correct methods of treatment and establish that adolescents are at increased risk of anemia, especially at younger ages (14-16 years). We have studied 200 pregnant women, 100 teenagers (study group) and 100 adult women (control group). In both groups we have investigated the level of iron, ferritin, and IL-3 in the blood serum. Iron-deficiency anemia was observed in the first trimester of pregnancy in 35% of pregnant adolescents. Usually the quantity of iron in the body during the first trimester is close to norm, but in our case, age and inadequate food intake in connection with the desire to be slim, play their role. Other clinical manifestations of anemia were not revealed. Iron deficiency anemia found in 22% of the adult group. Number of pregnant women with iron-deficiency anemia was considerably higher in both groups (adolescents and adults) in the third trimester, and quantity of ferritin was at the lower border of the norm. The need of iron usually increases up to 3mg/day in the second trimester and 3.5-4mg/day in the third trimester. In some women Level of IL-3 in the blood was normal (that indicate to the adequate hematopoiesis), serum iron quantity was at the lower border of the norm, Ferritin level was increased and clinical- laboratory indices revealed presence of infection. In our case the number of such patients was 28% among adolescents and 21% among adults. In other cases hematopoiesis was normal (IL-3 level was normal) and there were no signs of infectious disease, but clinical manifestations of anemia were still present which indicated to the presence of physiological anemia due to increased circulatory volume.
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PMID:[Pregnancy and iron, ferritin and IL-3 in the blood]. 1690 3

The purpose of this investigation was to determine whether echinacea supplementation results in alterations of erythroid growth factors and erythropoietic status. Twenty-four men age 24.9 +/- 4.2 y, height 1.7 +/- 0.8 m, weight 87.9 +/- 14.6 kg, and 19.3% +/- 6.5% body fat were grouped using a double-blind design and self- administered an 8000-mg/d dose of either echinacea (ECH) or placebo (PLA) in 5 x 400 mg x 4 times/d for 28 d. Blood samples were collected and analyzed for red blood cells (RBCs), hematocrit (Hct), hemoglobin (Hb), mean corpuscular volume, mean corpuscular hemoglobin content, prostaglandin E2, ferritin, erythropoietin (EPO), interleukin 3 (IL-3), and granulocyte-macrophage-colony-stimulating factor using automated flow cytometry and ELISA. ANOVA was used to determine significant differences (P ? 0.05). EPO was greater (P < 0.001) in ECH at Days 7, 14, and 21 and reflected a 44%, 63%, and 36% increase, respectively. IL-3 was greater (P = 0.011) in ECH at Days 14 and 21, which indicated a 65% and 73% increase, respectively. These data indicate that ECH supplementation resulted in an increase in EPO and IL-3 but did not significantly alter RBCs, Hb, or Hct.
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PMID:The effect of 4 wk of oral echinacea supplementation on serum erythropoietin and indices of erythropoietic status. 1796 12