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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies with protein tracers have shown that the luminal surface of the vascular endothelium of the bone marrow is endocytic. The endocytosis occurs through the formation of large bristle-coated vesicles (LCV). The anionic charge distribution in this process was examined at the luminal surface of the endothelial cell, At pH 1.8, colloidal iron (CI), native ferritin, and polycationic ferritin (PCF) are bound by the luminal surface of the endothelial cell, but not at the sites of LCV formation. PCF used over a pH range of 1.8--7.2 (CI is unstable at higher pH levels) revealed LCV binding of this agent in increasing manner from pH 3.5 upwards. PCF binding at low pH (1.8) at the endothelial cell surface was markedly reduced by neuraminidase. Neuraminidase did not reduce PCF binding by the endothelial cell surface nor by the LCV at higher pH levels. It is concluded that the luminal surface of the endothelial cell has exposed sialic acid groups which are absent or significantly diminished at endocytic sites. The free surface of the endothelial cells as well as the sites of endocytosis have, in addition, anionic material with a pKa higher than that of sialic acid (pKa 2.6). These anionic materials may be different at the sites of endocytosis as compared to those present at the free cell surface.
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PMID:Nonrandom distribution of sialic acid over the cell surface of bristle-coated endocytic vesicles of the sinusoidal endothelium cells. 2 50

Cell surface anionic sites on primary and transformed cultures of human vascular endothelium were studied using cationized ferritin (CF) as an ultrastructural marker. The native distribution of anionic sites on the upper (free) surfaces of cells, fixed in situ with glutaraldehyde, was uniform. Binding of the polycationic ligand, CF, in unfixed cells induced redistribution of anionic sites. Rapid formation of discrete patches of CF particles was followed by reappearance of binding between patches, movement of surface-bound CF into intercellular clefts, and endocytosis, over the next 30 min. Aldehyde-fixed cells, detached from the culture surface, bound CF on both upper and lower surfaces. The distribution and mobility of negatively charged membrane components in vascular endothelium may have relevance for thrombosis, atherogenesis, and vascular permeability.
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PMID:Distribution and movement of anionic cell surface sites in cultured human vascular endothelial cells. 46 14

Phagocyte-mediated oxidant damage to vascular endothelium is likely involved in various vasculopathies including atherosclerosis and pulmonary leak syndromes such as adult respiratory distress syndrome. We have shown that heme, a hydrophobic iron chelate, is rapidly incorporated into endothelial cells where, after as little as 1 h, it markedly aggravates cytotoxicity engendered by polymorphonuclear leukocyte oxidants or hydrogen peroxide (H2O2). In contrast, however, if cultured endothelial cells are briefly pulsed with heme and then allowed to incubate for a prolonged period (16 h), the cells become highly resistant to oxidant-mediated injury and to the accumulation of endothelial lipid peroxidation products. This protection is associated with the induction within 4 h of mRNAs for both heme oxygenase and ferritin. After 16 h heme oxygenase and ferritin have increased approximately 50-fold and 10-fold, respectively. Differential induction of these proteins determined that ferritin is probably the ultimate cytoprotectant. Ferritin inhibits oxidant-mediated cytolysis in direct relation to its intracellular concentration. Apoferritin, when added to cultured endothelial cells, is taken up in a dose-responsive manner and appears as cytoplasmic granules by immunofluorescence; in a similar dose-responsive manner, added apoferritin protects endothelial cells from oxidant-mediated cytolysis. Conversely, a site-directed mutant of ferritin (heavy chain Glu62----Lys; His65----Gly) which lacks ferroxidase activity and is deficient in iron sequestering capacity, is completely ineffectual as a cytoprotectant. We conclude that endothelium and perhaps other cell types may be protected from oxidant damage through the iron sequestrant, ferritin.
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PMID:Ferritin: a cytoprotective antioxidant strategem of endothelium. 151 45

We have investigated the effects of H2O2 (150 or 300 microM) on the ultrastructure and permeability of the pulmonary endothelium in rat lungs perfused for 60 min with buffered Hanks' bovine serum albumin medium. In one group of experiments, we examined the effect of H2O2 on the uptake and transport of cationized ferritin (CF) by endothelial cells in intra-acinar arteries, alveolar capillaries, and interlobular veins. The influence of the oxidant on endothelial adsorptive endocytic processes was assessed by measuring the density of ferritin particles in luminal vesicles, multivesicular bodies, and basal lamina. In a second group of experiments, we examined the effects of H2O2 on the fine structure and permeability to electron-dense macromolecules of arterial, microvascular, and venous endothelium. For this purpose, at the end of the 60-min perfusion with H2O2, CF was perfused to identify leaky vessels. We found that H2O2 caused a dose-dependent inhibition of transcytosis of CF in all vascular segments. At the lower dose of H2O2, inhibition of transcytotic activity was not associated with structural injury to the vascular endothelium or with elevation of wet-to-dry ratios. At the higher oxidant dose, inhibition of transcytosis was associated with leaky arterial endothelium and elevation of wet-to-dry ratios (6.44 +/- 0.12 vs. 5.64 +/- 0.16, P less than 0.02). The effects of H2)2 were prevented by adding catalase to the perfusate. The selective loss of structural integrity and leakiness of the arterial endothelium were diminished but not completely abolished by perfusing the oxidant retrograde from the venous side.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Leaky intra-acinar arteries in rat lungs perfused with hydrogen peroxide. 224 60

Cytochemical methods have been used to examine the vascular endothelium. With hemeproteins and immunocytochemistry, investigators have demonstrated the pathways that blood-borne molecules can take to gain access to the extravascular space (Ghitescu et al. 1986; Milici et al. 1987; Schneeberger and Karnovsky 1971; Simionescu et al. 1975). These same cytochemical methods have also provided evidence that morphologically similar endothelia may have different permeability properties (Hart and Pino 1985b, 1986; Pino 1985; Pino and Essner 1980, 1981). Differences in the location and chemical composition of cell surface moieties have been ascertained with enzyme digestion methods, lectins, and cationic ferritin (De Bruyn and Michelson 1978; Pino 1984c, 1986a, b; Simionescu et al. 1981a). The author hopes that he has provided the reader with representative examples of how investigators have used these cytochemical methods for their studies. As new methods are developed and applications are found for existing techniques such as ultracryomicrotomy (Milici et al. 1987) and colloidal gold markers (Pino 1987b), cytochemistry will remain a fundamental tool for the study of the structure and function of the vascular endothelium.
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PMID:Cytochemical studies of the vascular endothelium. 265 65

The surface reactivity of the dog heartworm (D. immitis) was evaluated by comprehensive contact angle measurements and a platelet retention test. Contact angle data yielded calculated surface energy terms very similar to those previously reported for intact vascular endothelium. The platelet test revealed the native worm surface to be nonreactive, retaining fewer platelets than glass or worms whose surfaces had been modified by extraction with acid and high salt solutions. The cuticular morphology of the heartworm was studied with both light and electron microscopy, the latter coupled with ferritin-conjugated double-layer immunolabeling to reveal adsorbed host protein on the cuticle surfaces. Multiple attenuated internal reflection (MAIR) IR spectroscopy confirmed the general composition of this surface layer to be glycoproteinaceous. Morphological and histochemical studies confirmed and extended previous descriptions of nematode cuticle, adding ultrastructural detail on cortical, medial, and basal layers. A trilaminar membrane, apparently corresponding to a mammalian cell membrane (plasmalemma), constituted the external cortical layer as observed in high magnifications. The existence of a glycocalyx of varying thickness was demonstrated in ruthenium red-stained sections. MAIR IR spectra showed this glycoproteinaceous film to appear, in fully hydrated samples, as a loose biological gel. Ferritin-antibody conjugate labeling confirmed the presence of adsorbed dog albumin, dog immunoglobulin class G (IgG) and dog complement fraction 3 (C3) in the cuticular surface layer. It is likely, therefore, that D. immitis heartworms demonstrate long-term thromboresistance at least in part due to their passive low-surface-energy overcoating with host proteins.
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PMID:Surface characterization of the cuticle of Dirofilaria immitis. 277 32

Sialic acid-bearing molecules on the luminal surface of the vascular endothelium in mouse and rat pancreatic capillaries were detected electron microscopically by using a procedure with ferritin hydrazide (FH), after preferential oxidation of sialyl residues with sodium periodate. The distribution of FH on the endothelial surface demonstrated the existence of microdomains with various densities of sialoglycoconjugates oxidizable by sodium periodate and accessible to the tracer. On the plasmalemma proper, FH binding sites were heterogeneously distributed. Their concentration on various microdomains decreased as follows: plasmalemma proper greater than coated pits greater than stomal diaphragms of plasmalemmal vesicles and transendothelial channels, and fenestral diaphragms. The membrane of plasmalemmal vesicles and transendothelial channels was not labeled by FH. Nonspecific binding of FH to the nonoxidized endothelial surface or that oxidized after neuraminidase treatment was relatively low.
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PMID:Distribution of sialoglycoconjugates on the luminal surface of the endothelial cell in the fenestrated capillaries of the pancreas. 398 74

The distribution and density of receptors for concanavalin A (Con A) on the surfaces of cells of intact and isolated popliteal and axillary lymph nodes were investigated in the rabbit. Intact lymph nodes were perfused via the subcapsular (marginal) sinus with either Con A peroxidase or Con A ferritin, fixed with glutaraldehyde, and processed for electron microscopy. Both Con A peroxidase and Con A ferritin were distributed on the plasmalemma of lymphocytes, macrophages, neutrophils, plasma cells, reticular endothelial cells, and the vascular endothelium. Counts of Con A-conjugated ferritin particles indicated that the density of Con A receptors was generally similar for lymphocytes, macrophages, and neutrophils but lower on plasma cells. When lymph node cells were isolated by mechanical methods and exposed to Con A ferritin, the label was homogenously distributed on the cell surfaces of most cells. However, Con A binding was significantly higher on the surface of isolated cells than in the intact node. It is suggested that the increase in density of Con A binding sites on isolated cells may possibly be due to an unmasking of cell surface moieties in which additional Con A receptor sites become available as a result of the isolation procedure. The density of Con A ferritin binding sites was also significantly lower on the surface of isolated plasma cells than the lymphocyte and macrophage, suggesting that the density distribution of cell surface saccharides is different for various lymphoid cells.
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PMID:Concanavalin A receptor sites on lymph node cells in vivo and in vitro. 629 43

Within the cranio-spinal cavity we can consider three compartments: blood, cerebro-spinal fluid and nervous parenchyma and thus, three barriers (Blood-Cerebro-Spinal Fluid, Blood-Brain, Cerebro-Spinal Fluid-Brain). The morphological studies of these barriers were performed with exogenous tracers such as horseradish peroxidase, cytochrome C and ferritin or endogenous tracers such as autologous antiperoxidase immunoglobulins. 1. The blood-brain barrier is exogenous and endogenous tracers proof. It is found on the level of the brain capillary endothelium with tight junctions and rare plasmalemmal vesicles. 2. The blood-cerebro-spinal fluid barrier is found on the level of choroid plexus and of leptomeningeal vessel. In the former, the tracer is stopped by the tight junctions (zonula occludens type) of the choroid plexus epithelium. Besides, there is no morphological evidence of transepithelial passage from blood to cerebro-spinal fluid. In the later, the barrier is, almost always, found on the level of the vascular endothelium. 3. The parenchymatous-cerebro-spinal fluid interface cannot be called a barrier because the diffusion of the tracers is not restricted either by the astrocytic marginal layer or by the ependyma. The circumventricular organs other than choroid plexus are morphologically characterized by the free diffusion of tracers in their perivascular connective space. Subcommissural organs capillaries alone behave like those of the brain. The spinal cord capillaries, in opposition to those of the brain, are characterized by a perivascular connective space, for 40 p. 100 of them. The significance of this fact is still unknown.
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PMID:[Hemato-encephalic barriers. Morphologic data]. 661 15

Histamine covalently bound to glutaraldehyde-activated ferritin was prepared as either monomers or as small aggregates of approximately 0.05 to 0.15 micrometer Diam, suitable for electron microscopic detection of histamine cellular binding sites. The histamine-ferritin conjugates (MF) maintain the histamine capability to induce the opening of endothelial junctions in venules. To investigate the distribution of histamine receptors in the vascular endothelium, monomers or aggregates of MF were perfused in situ (mice), and various vascular beds, particularly that of the diaphragm, were fixed and processed for electron microscopy. The conjugate was preferentially bound on restricted areas of luminal endothelial cell plasmalemma especially in regions rich in filaments, and near the junctions between endothelial cells. The density of histamine binding sites was characteristically high in venules; it occurred to a much lesser extent in arterioles, veins, and muscular arteries whereas capillaries and aorta showed the lowest values. A similar distribution was obtained after perfusion of H1 or H2 receptor agonists coupled to ferritin (2-pyridylethylamine-ferritin [PF], or 4-methylhistamine-ferritin [MF], respectively). The binding specificity was assessed through control experiments with either native or activated ferritin or by competition with histamine. The findings suggest that histamine receptors are largely represented in the cell membrane of the vascular endothelium, particularly in venules. Experiments using specific H1 and H2 receptor agonists (PF and MF) and antagonists (mepyramine and cimetidine) indicate that the venular endothelium contains mainly H2 receptors.
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PMID:Histamine receptors of the microvascular endothelium revealed in situ with a histamine-ferritin conjugate: characteristic high-affinity binding sites in venules. 720 74


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