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)

Prostaglandin and prostaglandin receptors were localized on unwashed ejaculate rabbit sperm utilizing ferritin conjugated antibody to prostaglandin. Reaction was obtained over the acrosomal portion of the plasma membrane, with a greater aggregation over the apex of the head. The remainder of the head plasmalemma and flagellum showed no deposits of of reaction product. The reaction did not occur if the sperm were washed prior to incubation with the labelled antisera. However enhanced binding of ferritin was demonstrated if washed sperm were pre-incubated in PGE1. No reaction was seen in similar studies with human sperm.
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PMID:Localization of prostaglandin on the plasmalemma of rabbit sperm. 4 69

The iron-binding proteins lactoferrin (LF) and H-ferritin have been implicated in the negative regulation of myelopoiesis in vitro and in vivo. The present studies evaluated the functional activity of affinity-purified LF from polymorphonuclear neutrophils (PMN) of patients with chronic myelogenous leukemia (CML) and LF/H-ferritin-cell interactions in a nonleukemic patient with LF deficiency with normal levels of circulating blood leukocytes. Affinity-purified CML-PMN-LF was found to be qualitatively deficient as a suppressor of the release of colony-stimulating factors from mononuclear blood cells, adding to previous information from our group documenting defective LF-cell interactions in CML. LF was detected by immunoradiometric assay in PMN of the patient with LF deficiency, but at a much lower level than normal. This LF was found, however, to be active as a suppressor molecular against the patient's cells and normal donor cells. Patient cells were as responsive as normal cells to effects of purified milk LF. Decreased LF levels in this patient were associated with increased levels of monocyte H-ferritin inhibitory activity, consistent with the known suppressive effects in vitro of LF on H-ferritin release from monocytes. Patient marrow hematopoietic progenitor cells were as responsive as progenitors from normal donors to suppression by purified H-ferritin and prostaglandin E1. These results are consistent with a role of LF and H-ferritin in the control of myelopoiesis in this patient.
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PMID:Qualitative functional deficiency of affinity-purified lactoferrin from neutrophils of patients with chronic myelogenous leukemia, and lactoferrin/H-ferritin-cell interactions in a patient with lactoferrin-deficiency with normal numbers of circulating leukocytes. 204 67

Polycationic derivatives of ferritin containing primary amino groups (CFah) or tertiary amino groups (CFdmp) were potent platelet agonists inducing shape change, aggregation and secretion, but also agglutination in the presence of EDTA. Pretreatment of platelets with neuraminidase, PGE1, indomethacin, or creatine kinase/creatine phosphate inhibited CF-induced activation. In contrast, neuraminidase and PGE1 increased the agglutination by CF, indicating an inverse relationship between activation and CF-induced agglutination. At pH 7.4, the cationic charges of CFdmp exceeded those of CFah by a factor of 1.5 and the platelets bound approximately 1.5 times more CFah than CFdmp, suggesting the same number of anionic surface sites for both CF preparations. The capacity of the platelets to bind CF was diminished by 55% at 0 degree C or by 62% after aldehyde fixation and by 13% with PGE1. This suggests that the binding capacity depends on the mobility of the binding sites in the plane of the membrane but is only slightly increased by platelet activation. Binding to fixed or cold platelets approached equilibrium within a few seconds whereas saturation required several minutes at 37 degrees C. Neuraminidase preferentially reduced the slow binding and much less the rapid binding. Since activation by CF developed during seconds, suppressible by a brief treatment with neuraminidase 25 mU/ml, a small portion of neuraminidase-sensitive sites appears to be necessary for CF-induced platelet activation. Full activation and agglutination occurred at CF concentrations far below saturating concentrations. The results show that neither CF-induced activation nor agglutination depend on a simple neutralization of the negative surface charge.
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PMID:Cationized ferritin as a platelet-stimulating surface probe. Binding to platelets and effects on platelet function. 308 60

Bone marrow cells from patients with leukemia, myelodysplastic syndromes, cancer, and other disorders on a phase I clinical trial with recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) were assessed in vitro for numbers of granulocyte-macrophage (CFU-GM), erythroid (BFU-E), and multipotential (CFU-GEMM) progenitor cells, and for growth patterns (colony-to-cluster ratio) of CFU-GM, cycling rates of CFU-GM, and responsiveness in vitro to colony-stimulating and colony-inhibiting factors. The colony-to-cluster ratio of CFU-GM and the dose-response curves of CFU-GM to stimulation by rhGM-CSF in vitro did not change during the clinical trial. However, the percentage of CFU-GM in DNA synthesis, which is a measure of the proliferative rates of these cells, determined by the high specific activity tritiated thymidine kill technique in vitro, was markedly enhanced in a reversible fashion after administration in vivo of rhGM-CSF. The increased cycling rates of CFU-GM were consistent with the induced increase in neutrophil counts in these patients that has been reported elsewhere. Additionally, marrow CFU-GM from patients given rhGM-CSF in vivo were increased in sensitivity to inhibition in vitro by recombinant human H-subunit (acidic) ferritin in two of eight cases, and were increased in sensitivity to inhibition by lower dosages of recombinant human tumor necrosis factor alpha in all patients evaluated. The sensitivity of CFU-GM to inhibition in vitro by recombinant human interferon gamma and prostaglandin E1 did not change during the clinical trial. These studies demonstrate that the rhGM-CSF is having an effect on CFU-GM in the patients on the phase I clinical trial. This information may be of significance in planning future clinical studies combining rhGM-CSF with chemotherapy and/or other biotherapy.
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PMID:Growth characteristics of marrow hematopoietic progenitor/precursor cells from patients on a phase I clinical trial with purified recombinant human granulocyte-macrophage colony-stimulating factor. 326 May 58

To clarify the clinical pictures of adult Still's disease, 228 cases reported in the past 15 years since Bywaters' first description were reviewed. These included our 9 new cases and an additional 25 cases from the Japanese literature, none of which had been described in previous English reviews. Most of the patients with long followup showed frequent recurrences. About one third developed deforming arthritis with ankylosis. There were 6 deaths. Of interest was the remarkably elevated levels of serum ferritin and prostaglandin E1 in some patients.
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PMID:Adult Still's disease: review of 228 cases from the literature. 272 61

A model of immune complex glomerulonephritis induced in mice by the daily injection of 4 mg. of apoferritin was used to examine the effect of administration of two prostaglandins, PGE1 and PGE2. The twice daily administration of either PGE1 or PGE2 in pharmacologic doses resulted in significantly less glomerular damage and a shift in the primary location of immune complex deposition from the capillary loops to the mesangium, as demonstrated by immunofluorescence and electron microscopy. The beneficial effect of the prostaglandins was associated with a significant decrease in antiapoferritin antibody levels. A separate study was performed to determine whether the mechanism of decreased antibody levels produced by PGE administration was related to a decrease in the number of plaque-forming cells (PFC). Mice received injections of saline, apoferritin, or apoferritin plus PGE2 for 9 days, and spleen cells were used to determine the number of direct and indirect PFC. No direct PFC were detected in any of the groups. There was no difference in the number of indirect PFC between mice receiving apoferritin and those receiving apoferritin plus PGE2 (98 +/- 13 versus 108 +/- 30), whereas mice receiving saline had no indirect PFC. The prevention of glomerular damage in immune complex glomerulomephritis and the shift in the site of complex deposition induced by PGE1 and PGE2 appear to be caused by reduction in specific antibody synthesis. This reduced synthesis is not related to an alteration in the number of antibody-producing cells.
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PMID:Suppression of antibody synthesis by prostaglandin E as a mechanism for preventing murine immune complex glomerulonephritis. 621 13

Washed and gel-filtered human platelets were dose-dependently aggregated by the addition of cationized ferritin (CF). Ca++ and plasma factors were not necessary to induce the aggregation. Immediately after the addition of CF, CF particles were attached to the surface of platelets that showed discoid form, as observed electron microscopically. Some platelets were connected to each other through the CF particles located on their membranes. After the addition of CF, the following was observed: at 15 sec after, platelets showed a round form and were aggregated to each other; at 3 min after, centralization of granules was clearly seen and the aggregates increased their size during the time course; at 3-5 min after, the CF-connected aggregates were found locally. Around the aggregates, other platelets were aggregated, though not through the membrane-located CF. Observing with a lumiaggregometer, the aggregation showed a biphasic curve associated with adenosine triphosphate (ATP) release. The second part of aggregation curve was inhibited by PGI2, PGE1, aspirin, N-ethylmaleimide, and apyrase. The first part of the aggregation curve was inhibited only by heparin. Neuraminidase treatment also inhibited the aggregation dose-dependently. These findings suggest that neutralization of the platelet surface negative charge by a positively charged macromolecule can trigger platelet aggregation, which is followed by the release reaction.
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PMID:Electron microscopic observations on platelet aggregation induced by cationized ferritin. 641 96

We studied the effect of PGE1 in pharmacologic doses on immune complex-induced glomerulonephritis produced by daily intraperitoneal injections of apoferritin. Mice received one of the following injection schedules: apoferritin 4 mg/day, apoferritin 4 mg/day plus PGE1 200 microgram twice daily, saline, or PGE1 200 microgram twice daily. Administration of apoferritin alone resulted in mesangial cell proliferation in all 14 mice with crescent formation in nine. Evidence of subepithelial and mesangial immune complex deposition and a significant increase in urine protein excretion was found. Treatment with PGE1 resulted in a mild increase in mesangial cells in six of 14 mice. No mice developed crescents on this regimen. In addition, proteinuria was prevented, and there was a marked diminution of immune complex deposition. Antiapoferritin antibody was detected in the sera of mice from both groups. No alteration in lymphocyte response to mitogen or in vitro PGE1 suppression of blastogenesis was detected. Our results indicate that PGE1 therapy alters immune complex glomerulonephritis in this model of murine chronic serum sickness by reducing glomerular immune complex deposition. However, no difference in specific or nonspecific immunologic responses was detected.
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PMID:Prostaglandin E1 therapy of murine chronic serum sickness. 699 40

Four hundred and sixty-seven hematopoietic stem cell transplantations (HSCTs) (217 autologous and 250 allogeneic HSCT) were performed in 374 children at four pediatric HSCT centers in Korea from January 2005 to December 2007. Among 467 transplants, veno-occlusive disease (VOD) developed in 72 transplants (15.4%) at a median of 10 days after HSCT. Multivariate analysis showed that BU or TBI-containing regimen (P=0.002), VOD prophylaxis without lipo-prostaglandin E1 (PGE1) (P=0.012), number of previous HSCT (P=0.014), and pretransplant serum ferritin (P=0.018) were independent risk factors for developing VOD. Mean serum ferritin levels were significantly higher in HSCT with VOD (2109.6+/-2842.5 ng/ml) than in HSCT without VOD (1315.9+/-1094.4 ng/ml) (P<0.001). The relative risk of death within 100 days of HSCT in transplants with VOD compared with transplants without VOD was 3.39 (confidence interval: 1.78-6.45). Our results suggest that lipo-PGE1 might have a protective effect against the development of VOD, and pretransplant serum ferritin could act as a risk factor for VOD. A larger prospective study is needed to confirm a possible role of lipo-PGE1 and iron chelation therapy in reducing the incidence of VOD.
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PMID:Hepatic veno-occlusive disease in children after hematopoietic stem cell transplantation: incidence, risk factors, and outcome. 2001 Aug 66