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 iron storage macrophage has been isolated from the marrow of Imferon-treated mice and studied in vitro by morphologic, histochemical, and functional tests and isotope labeling techniques. These macrophages on stained preparations are large, many times binucleate cells (up to 150 mu), and show Prussian blue reactivity. In Epon-embedded, stained thick sections they contain elongated narrow basophilic inclusions. These macrophages are actively phagocytic and pinocytic; histochemical studies show that these cells are rich in acid phosphatase, nonspecific esterase, and PAS diastase-resistant activity. Iron storage macrophages do not incorporate the 3H-thymidine. The electron microscopic appearance of this macrophage shows that the cell has ferritin free in the cytoplasm and several types of cytoplasmic granules: those with large quantities of electron-dense ferritin and/or hemosiderin (type A), elongated granules (type B) with moderately electron dense homogeneous matrix and some ferritin at the periphery, and granules with heterogeneous content (type C). The above findings demonstrate that the iron storage cell is a mature macrophage which contains hydrolases, ferritin, and a unique population of cytoplasmic granules which are lysosomal in nature. There is some evidence to suggest that the unusual lysosome (type B granule) occurs after macrophages have ingested erythrocytes.
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PMID:Morphologic and functional characteristics of bone marrow macrophages from imferon-treated mice. 4 60

The content of normal serum proteins, acute phase (C-reactive protein, pregnancy-associated alpha 2-glycoprotein) and tissue proteins (ferritin, nonspecific tissue esterase) was studied in the sputum of 256 patients with different pulmonary pathology, over time using immunochemical methods. Protein elimination with the sputum was shown to depend upon the nature and gravity of bronchitis and pulmonary destruction. Analysis of the qualitative composition of the sputum proteins and their content can be used in pulmonology for differential diagnosis and assessment of a course of pulmonary diseases.
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PMID:[Clinical significance of the immunochemical study of serum and tissue proteins of the sputum in pulmonary pathology]. 247 Jan 61

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

Monocytes infiltrate glomeruli during mesangial deposition of ferritin, and during experimental glomerulonephritis. To determine whether this is solely a local phenomenon, leucocyte infiltration in other organs has been studied following intravenous ferritin injection. Lewis rats received an i.v. injection of 150 mg ferritin/100 g body weight. At 24 h there was a peripheral blood leucocytosis (ferritin-treated rats 26.32 +/- 13.7, control rats 8.54 +/- 2.41 X 10(6) cells/ml) due to increase in polymorphs and monocytes. Bone marrow cell counts fell (ferritin-treated rats 49 +/- 7, control 80 +/- 11 X 10(6)/100 g body weight). Cell counts on cell suspensions of perfused, enzyme-digested lung, liver and spleen, and lung lavage showed major significant increases in total cell counts: lung 250 +/- 36 (89 +/- 16), lung lavage 2.6 +/- 0.8 (1.4 +/- 0.5), liver 140 +/- 37 (60 +/- 11), spleen 306 +/- 38 (200 +/- 27) X 10(6)/100 g body weight (control values in parentheses). Cytospin preparations of these suspensions, stained for non-specific esterase showed that the increase in cell numbers was due to increases in non-specific esterase-positive cells (monocytes) and polymorphs. These results demonstrate a generalized leucocyte mobilization, sequestration, and tissue infiltration after i.v. ferritin. The renal glomerulus therefore is not the only site of leucocyte accumulation. These findings may have relevance for studies on inflammation mediated by leucocytes in models of experimental immune complex glomerulonephritis.
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PMID:Blood leucocyte infiltration after intravenous injection of ferritin in the rat. 387 62

The relationship between Ia antigens on mouse resident peritoneal macrophages and the ability of lactoferrin (LF) to inhibit the production of granulocyte-macrophage colony stimulatory factors (GM-CSF) from these cells was investigated. Detection of the suppressive influence of LF on release of GM-CSF from greater than or equal to 10(5) macrophages/ml/plate required that the conditioned media being assessed for GM-CSF be prepared in the presence of indomethacin and/or be preincubated with anti-ferritin antiserum to respectively stop production of E-type prostaglandins and to remove acidic isoferritin-inhibitory activities that can mask the effects of LF. Treatment of mouse macrophages with monoclonal antibodies to the I-A and I-E/C subregions of Ia antigens in a complement C-dependent cytotoxicity assay killed less than 15% of the cells, but removed all Ia antigen+ macrophages and reduced GM-CSF production by approximately 50%. LF decreased GM-CSF production by untreated macrophages by approximately 50%, but had no effect on macrophages insensitive to treatment with anti-Ia plus C. Macrophages left at 37 degrees C for 5 and 24 hr were not killed by treatment with monoclonal anti-Ia plus C and GM-CSF production by these macrophages was not suppressed by LF. Treatment of macrophages with monoclonal anti-H-2K or anti-Mac-1 plus C reduced GM-CSF production greater than 95%. Anti-I-A, -I-E/C, -H-2K, or -Mac-1, in the absence of C, had no effect on viability of macrophages or on production of GM-CSF, but anti-I-A and -I-E/C each blocked the inhibitory action of LF. Lower concentrations of these antibodies could block the action of LF when anti-I-A and anti-I-E/C were mixed together better than when they were each used separately. The removal of Thy-1.2+ cells from unseparated or adherent peritoneal cells resulted in populations of cells that were up to 100% positive for nonspecific esterase, and did not influence GM-CSF production from these cells, the reduction of GM-CSF from these cells by LF, or the reduction of GM-CSF by the removal of Ia antigen+ cells. The results were similar whether or not T cells were removed from the assay marrow by treatment with antibodies Ly-1.1, Ly-2.2, and Qa4 plus C.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Lactoferrin acts on I-A and I-E/C antigen+ subpopulations of mouse peritoneal macrophages in the absence of T lymphocytes and other cell types to inhibit production of granulocyte-macrophage colony stimulatory factors in vitro. 614 10

Hemostatic function of 129 patients with cancer of the digestive system was studied on the clinical point of view. Activator (A) and inhibitor (I) of fibrinolysis of 94 cancer tissues were determined by Malone's method. The following results were obtained: Latent DIC state was observed in the patients with advanced stage. Great majority of the patients with PT less than or equal to 85%, antithrombin III (AT III) less than or equal to 25 mg/dl, FDP greater than or equal to 5 micrograms/ml, alpha 1 antitrypsin (alpha 1 AT) greater than or equal to 340 mg/dl, plasminogen (plg) less than or equal to 10 mg/dl and alpha 2 plasmin inhibitor (alpha 2 PI) less than or equal to 80%, were eligible only for non-curative operation on the preoperative evaluations. Persistent decreases in PT, AT III, plg and alpha 2 PI mean poor prognosis, which were seen within about 6 months prior to death. In gastric cancer patients, these abnormalities showed correlations with serum choline-esterase, albumin and ferritin, and post-operative changes of these parameters suggested the recurrence. There were I activities in the cancer tissues which were scarcely detected in the normal tissues. Some differences in A/I ratios were observed on types of organs involved, histological types and differentiative degrees. There were no correlations between the hemostatic state and A/I ratios. These results indicate the clinical usefulness of the hemostatic functions of the cancer patients and the fibrinolytic properties of the cancer tissues, and also suggested that tumor bearing state, liver function and non-specific stimulating mechanisms participate in the appearance of the abnormalities.
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PMID:[Hemostatic abnormalities of the patients with cancer. Clinical significance and fibrinolytic properties of the cancer tissues]. 620 15

Esteroproteinases extracted from the submandibular gland (SMG) of normal male mice were fractionated by isoelectric focusing into three major peaks with isoelectric point (pI) values of 9.9 (P-esterase), 5.8 (proteinase A), and 5.6 (proteinase D). In castrated males or normal females, an additional esteroproteinase with a pI of 4.6 (proteinase F) appeared. By single radial immunodiffusion analysis using a specific anti-proteinase F serum, the proteinase F content in females or castrated males was found to be 15 times as high as that in normal males. These facts suggest that the synthesis of proteinase F is inhibited by androgens. Immunocytochemical localization of proteinase F in the SMG was examined by indirect enzyme-labeled antibody and ferritin-labeled antibody methods for light and electron microscopy, respectively. Castration of normal males caused morphological changes in granular convoluted tubular (GCT) cells, i.e., GCT cells with both several small secretory granules in their apical region and some striations at their basal region (light cells) were observed in addition to typical GCT cells. Immunoreactive proteinase F was exclusively localized in such small secretory granules of the light cells, but was only minimally present in large secretory granules of the typical GCT cells. In females, however, uniform localization of proteinase F among secretory granules of all GCT cells was observed. It is suggested that the small secretory granules in light cells are formed after castration.
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PMID:Immunocytochemical study of proteinase F in the mouse submandibular gland. 642 27

To study human monocyte functions, we attempted to immortalize human monocytes by producing somatic cell hybrids between such monocytes and the mouse myeloma cell line NSI. In this study we report the successful establishment of eight hybrid cell lines that have been grown in culture for more than a year, and some of them retained part of the human chromosome complement, as well as monocyte markers and activities. Karyotype analysis of these hybrid lines revealed that cells of seven out of eight of the lines contained one to 16 human chromosomes and in four of them, more than nine human chromosomes were observed. Several of the cell lines expressed monocytic markers and functions. Thus, in two of the hybrid lines nonspecific esterase could be demonstrated in 10 to 29% of the cells, and Fc receptors were demonstrated in three of the hybrid cell lines. Significant levels of human ferritin were detected in one of the lines, and two other cell lines secreted interleukin 1-like substance into the culture medium. These results encourage us to use human-mouse somatic cell hybridization as an approach for the establishment of human monocyte cell lines, which will preserve their functions and produce monocyte-derived factors.
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PMID:Establishment of cell lines from somatic cell hybrids between human monocytes and mouse myeloma cells. 660 77

M cells in Peyer's patch follicle epithelium endocytose and transport luminal materials to intraepithelial lymphocytes. We examined (1) enzymatic characteristics of the epithelium covering mouse and rat Peyer's patches by using cytochemical techniques, (2) distribution of lectin-binding sites by peroxidase-labeled lectins, and (3) anionic site distribution by using cationized ferritin to develop a profile of M cell surface properties. Alkaline phosphatase activity resulted in deposits of dense reaction product over follicle surfaces but was markedly reduced over M cells, unlike esterase which formed equivalent or greater product over M cells. Concanavalin A, ricinus communis agglutinin, wheat germ agglutinin and peanut agglutinin reacted equally with M cells and with surrounding enterocytes over follicle surfaces. Cationized ferritin distributed in a random fashion along microvillus membranes of both M cells and enterocytes, indicating equivalent anionic site distribution. Staining for alkaline phosphatase activity provides a new approach for distinguishing M cells from enterocytes at the light microscopic level. Identical binding of lectins indicates that M cells and enterocytes share common glycoconjugates even though molecular groupings may differ. Lectin binding and anionic charge similarities of M cells and enterocytes may facilitate antigen sampling by M cells of particles and compounds that adhere to intestinal surfaces in non-Peyer's patch areas.
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PMID:Cytochemical analysis of alkaline phosphatase and esterase activities and of lectin-binding and anionic sites in rat and mouse Peyer's patch M cells. 665 Apr 35

In a previous publication the author and his co-workers demonstrated that atherosclerotic lesion development in the aorta of hypercholesterolemic pigs was preceded by intimal penetration of blood-borne mononuclear cells, and that medial smooth muscle cells were not involved in the formation of early fatty lesions in this model. The current study shows that aortic arch lesions do not progress beyond the fatty cell lesion stage for up to 30 weeks of a moderate cholesterol/lard diet, although they become more extensive in area. Mononuclear cells were found adherent to the endothelium, in endothelial junctions, and in the intima during this period, and were ultrastructurally identified as monocytes by the presence of peroxidase-positive granules (peroxisomes) in their cytoplasm. In addition, lesion areas with nonspecific esterase activity correlated well with Sudan IV staining. Intimal monocytes and altered intimal monocytes with an enlarged cytoplasm and containing a few lipid droplets were both shown to be phagocytic by their uptake of ferritin, which had penetrated the intima after intravenous injection. Circulating monocytes and those adherent to the endothelial surface did not contain ferritin in these animals. The results indicate that blood mononuclear cells associated with lesion formation in this model are, in fact, monocytes, which subsequently undergo transformation into macrophage foam cells in fatty streak lesions. The absence of medial cell involvement indicates that monocytes are the major foam cell precursor in these lesions.
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PMID:The role of the monocyte in atherogenesis: I. Transition of blood-borne monocytes into foam cells in fatty lesions. 723 61


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