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)

To investigate the relationship between hematopoiesis and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), we measured soluble TRAIL concentrations, reticulocytes, hemograms, and anthropometric variables in 156 healthy subjects. Serum TRAIL concentrations were analyzed by an enzyme immunoassay. Serum ferritin, thyroid hormone, total cholesterol, creatinine, and blood glucose levels were determined. There were no significant differences in blood cell counts and biochemical parameters between the subjects with TRAIL less than 63.5 pg/ml and TRAIL at least 63.5 pg/ml, nor between those with TRAIL at most 47.5 pg/ml (20th percentile) and TRAIL > or =80.9 pg/ml (80th percentile). However, hemoglobin, mean corpuscular hemoglobin (MCH), and MCH concentration (MCHC) averaged 15.6+/-0.8 g/dl, 31.9+/-1.1 pg, and 34.5+/-0.9 g/dl in the subjects with TRAIL at most 47.5 pg/ml, which were significantly above the values in those with TRAIL at least 80.9 pg/ml (14.7+/-0.9 g/dl, 30.4+/-1.3 pg, and 33.2+/-1.2 g/dl, P<0.05, respectively). Serum TRAIL levels were significantly higher in the subjects with decreased MCH than in those with elevated MCH. Soluble TRAIL concentrations were significantly correlated with hemoglobin (r=-0.25, P<0.05), MCH (r=-0.32, P<0.05), and MCHC (r=-0.29, P<0.05), but not correlated with leukocyte differentials and platelet counts. In conclusion, soluble TRAIL does not seem to influence leukocyte and platelet production but has an important relationship to erythropoiesis in healthy adults.
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PMID:Relationships between tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and hematopoietic activity in healthy adults. 1600 25

NF-kappaB/Rel transcription factors are best known for their roles in innate and adaptive immunity and inflammation. They also play a central role in promoting cell survival. This latter activity of NF-kappaB antagonizes programmed cell death (PCD) induced by the proinflammatory cytokine tumor necrosis factor (TNF)alpha and plays an important role in immunity, lymphopoiesis, osteogenesis, tumorigenesis and radio- and chemoresistance in cancer. With regard to TNFalpha, the NF-kappaB-mediated inhibition of PCD seems to involve an attenuation of the c-Jun-N-terminal kinase (JNK) cascade mediated through the induction of select downstream targets such as the caspase inhibitor XIAP, the zinc-finger protein A20, and the inhibitor of the MKK7/JNKK2 kinase, Gadd45beta/Myd118. Notably, NF-kappaB also blunts accumulation of reactive oxygen species (ROS), which themselves are pivotal elements for induction of PCD by TNFalpha, and this suppression of ROS formation mediates an additional protective activity recently ascribed to NF-kappaB. The antioxidant activity of NF-kappaB has been shown to depend upon upregulation of both Ferritin heavy chain (FHC)--a component of Ferritin, the primary iron-storage protein complex found in cells--and of the mitochondrial enzyme Mn++ superoxide dismutase (Mn-SOD). Indeed, the inductions of Mn-SOD and FHC represent another important means through which NF-kappaB controls proapoptotic JNK signaling triggered by TNFalpha. These findings might enable the development of new, more targeted approaches to treatment of diseases sustained by a deregulated activity of NF-kappaB, including some cancers and chronic inflammatory conditions.
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PMID:The NF-kappaB-mediated control of ROS and JNK signaling. 1626 88

Serum levels of T helper 1 (Th1)/T helper 2 (Th2) cytokines, angiogenic growth factors, and other prognostic factors were measured in 5 young adult patients with virus-associated hemophagocytic syndrome (HPS). Levels of 2 Th1 cytokines (interleukin [IL]-18 and tumor necrosis factor-alpha), 2 Th2 cytokines (IL-10 and IL-6), and 2 angiogenic growth factors (soluble intercellular adhesion molecule-1 and hepatocyte growth factor) were high in all of the patients examined, whereas those of Th1 cytokines such as IL-12 and macrophage inflammatory protein-1a were normal or low. Levels of IL-18 and IL-10 were highest in case 2, with a fatal outcome, and were lowest in case 4, with rapid recovery within 1 month. Although IFN-gamma levels were not elevated in 2 patients (cases 3 and 5), IL-18 levels were markedly high in both of these cases and the IL-6 level was highest in case 3. In contrast with the marked increase in the level of IL-10, the levels of IL-6, sIL-2R, and ferritin decreased rapidly and returned to normal within 2 months after therapy in case 3. The IL-18 level decreased somewhat, but remained elevated for 6 months, and the patient achieved a complete response within 11 months. Taken together, our findings suggest that both IL-18 and IL-10, but not IL-12, may play important roles in young adult patients with HPS via enhancing and suppressing Th1 immune responses, respectively.
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PMID:Serum levels of Thl/Th2 cytokines, angiogenic growth factors, and other prognostic factors in young adult patients with hemophagocytic syndrome. 1675 Nov 33

Previously, we have reported that there is a spatiotemporal relationship between iron accumulation in microglia and oligodendrocytes during normal development and in remyelination following injury. This in vivo observation has prompted us to develop a cell culture model to test the relationship between iron status of microglia and survival of oligodendrocytes. We found that conditioned media from iron-loaded microglia increases the survival of oligodendrocytes; but conditioned media from iron loaded activated microglia is toxic to oligodendrocytes. In the trophic condition, one of the proteins released by iron-loaded microglia is H-ferritin, and transfecting the microglia with siRNA for H-ferritin blocks the trophic response on oligodendrocytes. Lipopolysaccharide (LPS) activation decreases the amount of H-ferritin that is released from microglia and increases the release of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1. LPS activation of iron-enriched microglia results in the activation of NF-kB and greater release of cytokines when compared with that of control microglia; whereas treating microglia with an iron chelator is associated with less NF-kB activation and less release of cytokines. These results indicate that microglia play an important role in iron homoeostasis and that their iron status can influence how microglia influence growth and survival of oligodendrocytes. The results further indicate that ferritin, released by microglia, is a significant source of iron for oligodendrocytes.
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PMID:Cellular iron status influences the functional relationship between microglia and oligodendrocytes. 1695 88

This exploratory substudy of The Iron (Fe) and Atherosclerosis Study (FeAST) compared baseline inflammatory markers, including cytokines, C-reactive protein (CRP), and ferritin, in subjects with peripheral arterial disease (PAD) taking statins with subjects with PAD who were not taking statins. Inflammatory markers in the serum of 47 subjects with PAD not taking statins and a healthy cohort of 21 medication-free men were compared with 53 PAD subjects taking statins at entry to the FeAST. Healthy subjects demonstrated lower levels of tumor necrosis factor (TNF)-R1, interleukin-6 (IL-6), and CRP. TNF-alpha R1 averaged 2.28 ng/mL versus 3.52 ng/mL, p = .0025; IL-6 averaged 4.24 pg/mL versus 16.61 pg/mL, p = .0008; and CRP averaged 0.58 mg/dL versus 0.92 mg/dL, p = .0192. A higher level of IL-6 was observed in PAD statin takers versus PAD subjects not taking statins: 19.47 pg/mL versus 13.24 pg/mL, p = .0455. As expected, total cholesterol and low-density lipoprotein levels were lower in the statin-treated group, p = .0006 and p = .0001, respectively. No significant differences in inflammatory cytokines were detected for varying doses of simvastatin. Additionally, no significant differences in inflammatory biomedical markers were found in subjects with PAD alone compared with those with concomitant coronary artery disease (CAD). Unexpectedly, serum inflammatory cytokine IL-6 levels were significantly higher in PAD subjects receiving statins. There was no difference in measured inflammatory markers in PAD subjects with concomitant CAD.
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PMID:Statins and biomarkers in claudicants with peripheral arterial disease: cross-sectional study. 1702 9

In the present study, turpentine oil was injected in the hind limb muscle of the rat to stimulate an acute-phase response (APR). The changes in the gene expression of cytokines and proteins known to be involved in the iron regulatory pathway were then studied in the liver and in extra-hepatic tissue. In addition to the strong upregulation of interleukin-6 (IL-6) and IL-1 beta observed in the inflamed muscle, an upregulation of the genes for IL1-beta and tumor necrosis factor-alpha, but not IL-6, were detectable in the liver. Hepatic Hepc gene expression increased to a maximum at 6 h after the onset of APR. An upregulation of transferrin, transferrin receptor 1 (TfR1), TfR2, ferritin-H, iron responsive element binding protein-1 (IRP1), IRP2 and divalent metal transporter gene expression was also found. Hemojuvelin (Hjv)-, ferroportin 1-, Dcytb-, hemochromatosis-gene- and hephaestin gene expression was downregulated. Hepcidin (Hepc) gene expression was not only detectable in extra-hepatic tissues such as heart, small intestine, colon, spleen and kidney but it was also upregulated under acute-phase conditions, with the Hjv gene being regulated antagonistically. Fpn-1 gene expression was downregulated significantly in heart, colon and spleen. Most of the genes of the known proteins involved in iron metabolism are expressed not only in the liver but also in extra-hepatic tissues. Under acute-phase conditions, acute-phase cytokines (eg IL-6) may modulate the gene expression of such proteins not only in the liver but also in other organs.
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PMID:Changes of gene expression of iron regulatory proteins during turpentine oil-induced acute-phase response in the rat. 1741 67

Adult Still's disease (ASD) is a systemic rheumatic disease characterized by high spiking fever, erythema, polyarthritis, and increased levels of C-reactive protein, ferritin, and interleukin (IL)-18. Recently, biological agents targeting proinflammatory cytokines such as tumor necrosis factor (TNF) alpha, IL-1, and IL-6 have been described as effective treatments for refractory ASD. Herein, we present a patient with ASD, who was successfully treated by tacrolimus concomitant with corticosteroid, while infliximab and etanercept were not effective. Tacrolimus may be one of the drugs for the ASD patients refractory to the conventional treatments including TNF inhibitors.
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PMID:Successful treatment of a patient with refractory adult Still's disease by tacrolimus. 1743 76

Hepcidin is a principal iron regulatory hormone and its expression is stimulated by cytokines. The aim of this study was to determine serum levels of the prohormone form of hepcidin, pro-hepcidin, in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The study included 72 RA and 28 SLE patients and 33 healthy controls (HC). Serum iron status, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and pro-hepcidin levels were determined. Pro-hepcidin levels in the RA group was higher than SLE and HC groups (p < 0.05, p < 0.001, respectively). Pro-hepcidin levels did not correlate with disease activity scores, cytokine levels and serum iron status in the RA and SLE groups, while it correlated with TNF-alpha, IL-6 and ferritin levels in the HC group (r = 0.459, p < 0.01, r = 0.374, p < 0.05, r = -0.603, p < 0.01, respectively). Pro-hepcidin levels show extremely wide variations within the groups as do iron status and cytokines. Despite these wide variations correlation analysis do not reveal anything.
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PMID:Serum pro-hepcidin levels in rheumatoid arthritis and systemic lupus erythematosus. 1827 47

Controlling iron/oxygen chemistry in biology depends on multiple genes, regulatory messenger RNA structures, signaling pathways and protein catalysts. Ferritin synthesis is regulated by cytokines (tumor necrosis factor-alpha and interleukin-1alpha) at various levels (transcriptional, post-transcriptional, translational) during development, cellular differentiation, proliferation and inflammation. The cellular response by cytokines to infection stimulates the expression of ferritin genes. The immunological actions of ferritin include binding to T lymphocytes, suppression of the delayed-type hypersensitivity, suppression of antibody production by B lymphocytes, and decreased phagocytosis of granulocytes. Thyroid hormone, insulin and insulin growth factor-1 are involved in the regulation of ferritin at the mRNA level. Ferritin and iron homeostasis are implicated in the pathogenesis of many disorders, including diseases involved in iron acquisition, transport and storage (primary hemochromatosis) as well as in atherosclerosis, Parkinson's disease, Alzheimer disease, and restless leg syndrome. Mutations in the ferritin gene cause the hereditary hyperferritinemia-cataract syndrome and neuroferritinopathy. Hyperferritinemia is associated with inflammation, infections and malignancies, and in systemic lupus erythematosus correlates with disease activity. Some evidence points to the importance of hyperferritinemia in dermatomyositis and multiple sclerosis, but further mechanistic investigations are warranted.
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PMID:Hyperferritinemia in autoimmunity. 1830 May 83

Uremic pruritus is one of the common complications in long-term dialysis patients. Recently, researchers reported that immunohypothesis with high serum level of cytokines could be the cause of uremic pruritus. Polymethylmethacrylate (PMMA) artificial kidney (AK) has been reported to adsorb more serum cytokines than other high-flux AKs. In July 2006, 30 patients with severe uremic pruritus from 300 chronic hemodialysis (HD) patients in a single center entered this prospective study. Their dialyzers were changed to PMMA AK for 4 weeks. The severity of pruritus was evaluated every week using the results of a questionnaire (pruritus score). Laboratory assays including predialysis serum blood urea nitrogen (BUN), creatinine, beta2-microglobulin (beta2M), calcium, phosphate, intact parathyroid hormone (iPTH), total CO(2), ferritin, hematocrit, high-sensitivity C-reactive protein (hsCRP), IL-1beta, IL-2, IL-6, IL-18, tumor necrosis factor-alpha (TNF-alpha), Kt/V, and beta2M clearance were measured before and at the end of 4 weeks of PMMA AK use. PMMA AK was effective in reducing the pruritus score from 23.46 +/- 11.94 to 7.38 +/- 6.42 (P < 0.001). The effect of uremic pruritus relief appeared after 1 week of PMMA AK use. There were no significant differences in the laboratory assay results including predialysis serum BUN, Cr, beta2M, calcium, phosphate, calcium-phosphate product, iPTH, total CO(2), ferritin, hematocrit, hsCRP, IL-1beta, IL-2, IL-6, IL-18, TNF-alpha, Kt/V, and beta2M clearance. The mechanism for the beneficial effect of PMMA AK on uremic pruritus remains to be determined. PMMA AK may be a useful adjuvant therapy in chronic HD patients with severe uremic pruritus.
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PMID:Uremic pruritus, cytokines, and polymethylmethacrylate artificial kidney. 1842 97


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