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 presence of uniform negative charges on the surface of cultured rat glomerular mesangial cells was demonstrated by an ultrastructural marker, cationized ferritin. Interaction between cell surface negative charges and protamine sulfate, stimulated the synthesis of prostaglandins E2, F2 alpha, 6-keto-PGF1 alpha and thromboxane B2 (TXB2) in a dose-dependent manner, reaching a maximum response at protamine concentration of 50 micrograms/ml. The effect of protamine sulfate was reversed by 25 units/ml heparin. The polyanions, L-glutamic and L-aspartic acids, reversed the protamine effect in a dose-dependent manner. Excess substrate, arachidonic acid, masked the protamine sulfate-stimulated PGE2 synthesis by mesangial cells. The effect of protamine sulfate on PGE2 synthesis was rapid, peaked in 5 min and was independent of extracellular Ca2+. A synthetic cation, poly(L-lysine) hydrobromide, exerted a similar effect on cellular PGE2 synthesis in mesangial cells. The effect of poly(L-lysine) was dependent on the molecular mass of the cationic species employed and was maximum at 17 to 90 kDa. The use of large molecular mass polymers of L-lysine (175 and 565 kDa) resulted in a decline in PGE2 synthesis. These observation indicate that, in mesangial cells, changes in cell membrane electrical charge are linked to enhanced biosynthetic activity and eicosanoid synthesis.
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PMID:Effect of polycations on prostaglandin synthesis in cultured glomerular mesangial cells. 240 12

Foamy alveolar macrophages (FAM) are observed in lungs injured by Bleomycin (BLM), but their relation to pulmonary fibrosis is not clearly understood. We purified FAM from BLM-instilled rat lungs by density gradient centrifugation on Percoll, and studied the effect of FAM on pulmonary fibrosis. The cells lavaged from the rat lungs 14 days after the administration of BLM (B) or saline (S), were applied on Percoll. After centrifugation, the cells layered on each interface were collected and named as SI, SII, SIII, and BI, BII, BIII in order of gravity. The BI layer included 8.5% of unfractionated cells (U). These BI cells were viable (88%), significantly larger than the others, nonspecific esterase positive cells, and included much ferritin and lysozyme, and were morphologically identified as alveolar macrophages (AM). Therefore, we called the BI cells FAM. We estimated the capacity of FAM (2.5 X 10(5] to synthesize DNA (3H-thymidine uptake) and RNA (3H-uridine uptake), and the activities of silica-stimulated FAM to cause proliferation of mouse thymocytes (IL-1 activity) and rat lung fibroblasts (FP activity), and to produce PGE2. FAM has a lower mitogenic activity but did not have been protein synthetic activity as compared with the others. Silica-stimulated FAM released less IL-1 than BII or BIII, and induced less fibroblast growth than BII, but induced as much as BIII, possibly because of the increased capacity of BIII cells to produce PGE2, which is known to inhibit fibroblast growth. In this way, FAM were considered to be "already activated" rather than "highly activated" cells, but the presence of FAM suggested that smaller or denser AM might receive bleomycin stimulation and release fibrogenic mediators (IL-1 or MDGF) into the alveolar spaces during FAM formation, and that AM might participate in the fibrogenic responses.
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PMID:[The effect of foamy alveolar macrophages presented in bleomycin-injured rat lungs in pulmonary fibrosis]. 247 35

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

The bronchoalveolar lavage (BAL) is considered a basic technique as a diagnostic aid in Pneumology. However, one of the main problems faced by the clinician is the lack of standardization of the technique. This has been resolved through the drafting of international standards. The other problem is the lack of what might be called a "reference" BAL. In order to establish a reference BAL, we analyzed 203 BAL divided in two groups: a control group and a pathologic group, make up by extrinsic asthma, intrinsic asthma, pulmonary infections, diffuse interstitial pneumopathies, bronchopulmonary tumors and chronic bronchitis. We have studied both the cytologic and the biochemical component of the BAL. Among the biochemical markers, we have considered; carcinoembrionary antigen (CEA), tissular polypeptidic antigen (TPA), neuronal specific enolase (NSE), ferritin (FER), calcitonin (CT), ACTH, histamin (HIS) and prostaglandin (PGE2). In order to establish the reference values, we have used the modified Baye's theorema. The BAL that we obtained was the following: volume 20 ml, cells 35 x 10(5) cells/ml, macrophages 77%, lymphocytes 22%, neutrophils 4%, eosinophils 2%, CEA 14 ng/mg, TPA 84 U/g PT, NSE 5 ng/mg PT, FER 42 ng/mg PT, CT 15 pg/mg PT, ACTH 51 pg/mg PT, HIS 1.22 ng/mg PT, PGE2 35 pg/mg PT.
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PMID:[Cytologic and biochemical component in 203 bronchoalveolar lavages. Reference values]. 771 15