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 and localization of antigenic sites in glomeruli of 14 patients with acute poststreptococcal glomerulonephritis (AGN) were studied by immunofluorescein and immunoferritin technics. Labeled IgG fractions from the same patients were used for the identification of antigenic sites. The staining capacity of these IgG fractions depended on the time when sera were obtained. Staining was minimal during the first week, and increased up to the fourth or fifth week. Glomeruli, however, stained only when renal tissue was obtained during the early phase of the disease. Precise localization of antigenic sites was determined with ferritin-conjugated patients' IgG. Segmental deposition of ferritin was observed in the mesangial matrix and on the endothelial side of the glomerular basement membrane. Subepithelial electron-dense deposits contained no or very few ferritin particles. In contrast, ferritin-conjugated antihuman IgG was distributed diffusely in the mesangial matrix, on the endothelial side of the basement membrane and in subepithelial deposits. These findings suggest that, during the early stage of acute poststreptococcal glomerulonephritis, free antigen is present in the glomeruli of patients with this disease.
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PMID:Demonstration of antigenic sites in glomeruli of patients with acute poststreptococcal glomerulonephritis by immunofluorescein and immunoferritin technics. 411 83

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

We studied the effect of the administration of different doses of antigen in a model of chronic glomerulonephritis produced in mice by the daily injection of apoferritin. Four groups of mice received intraperitoneal injections of 4 mg apoferritin (group 1), 2 mg apoferritin (group 2), 1 mg apoferritin (group 3), or saline (group 4) daily. Significant proteinuria and the presence of antiapoferritin antibody were demonstrated in mice immunized with apoferritin. The severity of histologic damage and the extent of staining for IgG significantly increased with larger doses of apoferritin. Electron microscopy revealed subepithelial and mesangial electron-dense deposits. Administration of large daily doses of apoferritin to mice results in a reliable model of immune complex glomerulonephritis and crescent formation.
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PMID:Chronic serum sickness in the mouse. Relationship of antigen dose to glomerular pathology. 621 78

Immune-complex-mediated glomerulonephritis (IC-GN) was induced with daily intraperitoneal injections of horse apoferritin (HAF) for varying intervals in Swiss albino and BALB/c mice. Anti-HAF antibody avidity in plasma pools from mice with predominantly mesangial immune deposits was compared with avidity in plasma pools from mice with predominantly capillary wall deposits. Plasma from Swiss mice having predominantly mesangial deposits after 7 or 14 days of HAF had higher avidities than plasma from Swiss mice with predominantly capillary wall deposits after 14 days or more than 28 days of HAF. Plasma from BALB/c mice with exclusively mesangial deposits after 7 days of HAF had higher avidity than plasma from BALB/c mice with predominantly capillary wall deposits after 14 or more days of HAF. Therefore, there was a correlation between glomerular site of immune deposition and avidity of circulating anti-HAF antibodies, with higher avidity antibodies associated with mesangial immune deposits and lower avidity antibodies with capillary wall deposits.
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PMID:Influence of antibody avidity on glomerular immune complex localization. 622 26

We investigated the pathogenesis of increased glomerular permeability in Balb/c mice after 5 weeks of administration of a polyclonal B cell activator (bacterial lipopolysaccharide). The glomerular transfer of anionic ferritin across the capillary walls and the urinary excretion of serum albumin served as probes of glomerular permeability; anionic groups of the glomerular basement membrane were assessed by the binding of cationized ferritin, and glomeruli were studied by light, immunofluorescence, and electron microscopy. The mice developed circulating immune complexes, proteinuria, and a proliferative glomerulonephritis, with mesangial and capillary loop deposits of immunoreactants. Increased transfer of anionic ferritin molecules occurred across capillary walls with and without demonstrable electron-dense deposits; detachments of visceral epithelium were not seen, and epithelial transport of anionic ferritin was negligible. Loss of anionic groups was extensive in glomerular capillary loops with and without associated electron-dense deposits. The findings indicate that an increase in glomerular permeability may precede the deposition of immunoreactants in the capillary wall; that filtration of macromolecules can occur across capillary walls with or without demonstrable immune deposits; and that loss of anionic groups of the glomerular basement membrane and enhanced filtration of macromolecules can occur in the absence of focal detachments of the visceral epithelium.
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PMID:Altered glomerular permeability in the early phase of immune complex nephritis. 622 69

Hypertension frequently accompanies chronic glomerulonephritis. Mesangial injury and glomerulosclerosis are common in glomerulonephritis and are often harbingers of progressive glomerular destruction. Thus, in a model of mesangial immune injury we studied the relationship between hypertension, mesangial injury, and glomerulosclerosis. We induced mesangial ferritin-antiferritin immune complex disease (FIC) in Dahl salt-sensitive (S) and salt-resistant (R) rats. S and R rats with FIC were fed chow containing 0.3% NaCl until 14 weeks of age and then switched to 8.0% NaCl chow until 28 weeks of age. Groups of control S and R rats (no FIC) were either fed 0.3% NaCl for 28 weeks or switched to 8.0% NaCl chow at 14 weeks of age. Blood pressure, serum creatinine, urinary protein, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined at 14 and 28 weeks of age. R rats with or without FIC did not develop hypertension; mesangial injury was minimal. At 14 weeks of age, only S FIC rats developed hypertension, proteinuria, significant mesangial expansion and early glomerulosclerosis. At 28 weeks of age, proteinuria, mesangial expansion, and glomerulosclerosis were significantly more severe in hypertensive S rats with FIC than in those without FIC. These studies show that despite a normal salt intake, mesangial injury hastened the onset of hypertension, but only in rats genetically predisposed to hypertension (S FIC at 14 weeks). High dietary salt further aggravated hypertension, which, in turn, magnified both mesangial injury and glomerulosclerosis. Clinically, the different rates of progression of human glomerulonephritis associated with hypertension may be in part dependent on similar mechanisms.
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PMID:Mesangial immune injury, hypertension, and progressive glomerular damage in Dahl rats. 623 58

Genetically disparate inbred mouse strains mounting quantitatively different immune responses to a potentially nephritogenic heterologous protein had varied development of glomerulonephritis (GN) dependent upon the interaction between level of antibody response and antigen dose. High responder BALB/c mice given high doses of horse apoferritin developed a severe necrotizing GN. BALB/c mice given low dose horse apoferritin developed less severe GN, or when antibodies were in extreme excess, no GN. Low responder C3H mice given high dose horse apoferritin were in extreme antigen excess and developed no GN. C3H mice given low dose horse apoferritin developed a glomerulopathy characterized by capillary loop immune deposits. Interstrain differences in immune clearance and avidity did not account for this varied nephritogenicity, although avidity did relate to glomerular site of immune deposits in the BALB/c model. In the models under consideration susceptibility to heterologous antigen-induced glomerular injury was a function of the magnitudes of both the antibody response and the antigenic challenge.
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PMID:Interaction of antigen load and antibody response in determining heterologous protein nephritogenicity in inbred mice. 634 22

The charge-based barrier of the glomerular capillary filter was investigated in normal mice and in mice with immune complex lupus nephritis. Cationized ferritin (CF), pI 7.7 To 8.5, was used as a molecular probe of fixed anionic sites. Mice with various degrees of proteinuria and severity of glomerulonephritis were systemically injected with CF and their glomeruli studied ultrastructurally employing morphometric methods. A decreased and erratic localization of CF was observed in the lamina rara externa, in the intervening basement membrane between immune deposits, and in basement membrane projections, areas previously shown to be abnormally permeably to a large anionic protein. In small numbers, CF molecules were found in residual epithelial slits and in the urinary space. In normal mice, CF regularly labeled the laminae rarae of the glomerular basement membrane and the slit pore area but not leak into the urinary space. Such differences in CF localization in capillary loops of proteinuric and normal mice were confirmed by morphometric estimate of particle counts. Focal areas of increased permeability to anionic protein are deficient of and/or exhibit a disorderly redistribution of fixed anionic sites.
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PMID:Glomerular permeability: focal loss of anionic sites in glomeruli of proteinuric mice with lupus nephritis. 644 31

Swiss albino, BALB/c, and eight substrains of C3H mice were given daily intraperitoneal injections of horse apoferritin (HAF) for up to 56 days. At varying intervals, renal tissue was examined by light, immunofluorescence, and electron microscopy. Swiss mice developed proliferative glomerulonephritis after 7 to 14 days of HAF, and 45 per cent progressed to severe crescentic glomerulonephritis after from 21 to 56 days of HAF. In Swiss mice, glomerular immune deposits evolved from predominantly IgM mesangial deposits at 7 days to mesangial IgG at 14 days to capillary wall IgG after 21 or more days of HAF injections. BALB/c mice given identical HAF doses never developed severe crescentic glomerulonephritis but rather an extensive global necrotizing glomerulonephritis most prevalent after from 9 to 18 days of HAF. The distinct evolution of glomerular immune deposits observed in Swiss mice was less clear-cut in BALB/c mice, with greater persistence of mesangial deposits and IgM over time. Only 11 per cent of C3H mice (confined to two substrains) developed glomerular lesions by light microscopy after 2 to 3 weeks of HAF administration. No C3H/HeN mice developed glomerulonephritis even after up to 47 days of HAF injection. From 7 days on, 45 per cent of HAF-injected C3H mice had low level IgM mesangial immune deposits but did not manifest the evolution from mesangial to capillary deposition observed in BALB/c and Swiss albino mice. F1 hybrid and congenic mice carrying BALB/c H-2 genetic information developed glomerular lesions similar to those produced in BALB/c mice. These data (1) indicate an interrelated morphologic and immunohistologic evolution of heterologous protein induced glomerular lesions in mice, (2) demonstrate morphologic and immunohistologic differences in glomerular lesions development between genetically disparate mouse strains given identical antigen exposures, and (3) support the genetic control of heterologous protein-induced glomerulonephritis and suggest a role for the major histocompatibility region in this genetic regulation.
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PMID:Interstrain variations in nephritogenicity of heterologous protein in mice. 646 Aug 98

A model of immune complex glomerulonephritis (ICGN) produced in mice by the daily injection of apoferritin was employed to study the effect of treatment with various doses of prostaglandin E2 (PGE2) on glomerular damage, immune complex deposition, proteinuria, and serum anti-apoferritin antibody. Administration of PGE2, 200 micrograms twice daily, resulted in a significant decrease in glomerular damage and immune complex deposition, prevented the development of proteinuria, and significantly reduced serum levels of anti-apoferritin antibody. PGE2, 100 micrograms twice daily, resulted in a decrease in immune complex deposition as assessed by immunofluorescence microscopy, but this dosage did not significantly alter glomerular damage, proteinuria, or antibody levels. PGE2 dosages of 50 and 25 micrograms twice daily had no effect on any of these parameters. The protective effect of PGE2 on the development of ICGN occurred only at dosages that were associated with decreased anti-apoferritin antibody.
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PMID:Treatment of murine immune complex glomerulonephritis with prostaglandin E2: dose--response of immune complex deposition, antibody synthesis, and glomerular damage. 657 81


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