Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the effect of biochemical modifications not possible in vivo, filters of dog glomerular basement membrane (GBM) were constructed in ultrafiltration cells in vitro. The sieving coefficients (SCs) of three protein markers of differing size and charge (native, anionic bovine albumin-BSA; cationized BSA-cBSA; and immunoglobulin G-IgG) were determined using filters of differing amounts of control GBM, and under varying transmembrane pressures (delta P). Flow rates did not increase proportionately with increasing delta P, indicating filter compressibility. Protein SCs did not change with changing delta P, but did decrease with increasing filter thickness. Control filters showed a small but definite charge selectivity (SCcBSA++ - SCBSA greater than 0); a much greater degree of size selectivity (SCcBSA - SCIgG) was observed. Hexadimethrine (HDM), a polycation which causes proteinuria in vivo, led to marked increases in protein SCs. In contrast, removal of the major population of intrinsic GBM negative charges by carboxyl group methylation only produced a small increase in the filtration of BSA, with no change in filtration of cBSA or IgG. Other biochemical modifications (heparinase or neuraminidase treatment) had no effect on filter permselectivity. Carboxyl group methylation essentially abolished filter binding of cationized ferritin, which showed substantial binding to control filters. These in vitro studies provide confirmatory evidence for a direct effect of HDM on the permselective properties of GBM. In addition, biochemical modification studies suggest a fundamental difference between the binding of an exogenous polycation to GBM anionic sites and the removal of intrinsic charges.
 ...
PMID:Macromolecular sieving by glomerular basement membrane in vitro: effect of polycation or biochemical modifications. 207 68

Serum sickness nephritis was induced in Fisher rats by immunization with egg albumin (EA) and correlations between immune complex deposition, alterations of podocytes and development of proteinuria were analysed. Immunoelectron microscopy showed that EA, rat IgG and C3 were confined to the electron-dense deposits (Ds). From 3 weeks, when significant proteinuria had developed, the subepithelial region was filled with large numbers of Ds on the peripheral capillary wall as well as in the paramesangium. The loss of slit diaphragms and detachment of foot processes overlying Ds were observed and the escape of Ds into urinary space was frequently detected. Morphometric evaluation showed that the volume of subepithelial Ds and the number of the sites of podocytic detachment correlate significantly with the amount of proteinuria. In addition, the native ferritin injected via the abdominal aorta was seen in large amounts in the urinary space near the areas devoid of epithelial covering. The development of podocytic detachment was clearly coincident with the appearance of proteins with a larger molecular weight in urine. From these results, it is suggested that the loss of slit diaphragms and the detachment of podocytes resulting from the progressive accumulation of Ds will allow the leakage of proteins of larger molecular weight across the capillary wall. These podocytic lesions may be one of the main aetiologies for the development of heavy proteinuria in this model.
 ...
PMID:Sequential ultrastructural podocytic lesions and development of proteinuria in serum sickness nephritis in the rat. 214 98

In situ immune complex glomerulonephritis can be induced in the rat employing cationized antigen planted in the glomerular basement membrane (GBM) as a target for specific antibody. Another possible mechanism of in situ immune complex formation is antibody already present in the GBM to bind circulating antigen. Present study was performed in order to determine whether cationized antibodies planted in the GBM could react with anionic as well as cationic antigens to form immune deposits. Horse ferritin, rabbit antibody to horse native ferritin (f-Ab) and rabbit antibody to ovalbumin (o-Ab) were highly cationized as described by Danon et al. The ability of the cationized antibodies to precipitate antigens was estimated by Ouchterlony analysis. 500 micrograms/100 g body weight (b.w.) of cationized f-Ab or o-Ab was perfused into the left renal artery of male Wistar rats and 0.1-10.0 mg/100 g b.w. of either native or cationized ferritin or ovalbumin was injected respectively into the tail vein 1 hr later. Estimation of proteinuria was done and the kidneys were removed up to 5 days for immunohistological as well as electron microscopical examination. Cationized antibodies bound to anionic sites of the GBM and combined with subsequently injected cationized ferritin or native ovalbumin in situ, both leading to formation of subepithelial immune deposit with activation of C3 and caused mild proteinuria. Native ferritin, however, induced neither subepithelial immune deposit nor proteinuria, because it didn't permeate through the GBM. The presented model indicates that antibody molecules of high positive charge can bind to the GBM and react with specific antigens that are traversing the barrier to form immune deposits. This is independent of the charge of antigen provided that the antigen molecules are permeable into the GBM, as is the case with ovalbumin but not native ferritin.
 ...
PMID:[In situ immune complex glomerulonephritis induced by perfusion of cationized antibody]. 228 98

In the syncytiotrophoblastic surface of the toxemic full-term placentae, the sialates and their consequent negative charging were studied by both electron microscopic histochemistry (Ferritin method) and Western blot analysis. Evidence is presented showing (1) that the reactions with both the ferritin labelled Limulus Polyphemus Agglutinin (LPA-ferritin), specific to sialates, and the cationized ferritin, specific to a negative charge, decrease in the specimens of toxemic placentae, (2) that the density of sialates in placentae of severe gestational proteinuria or/and hypertension is statistically lower than that of severe gestational edema, and (3) that there is no difference between the blotted bands in normal placentae and toxemic ones regardless of the severity of the toxemia. These results indicate that the reduction of the surface negative charging is demonstrated in toxemic syncytiotrophoblasts and appears to be secondary to the decrease in the amount of sialate.
 ...
PMID:Sialates and negative charge on the surface of syncytiotrophoblastic cells of full-term placentae in toxemic patients. 233 76

Proteinuria and progressive glomerulosclerosis are commonly associated with nephron loss. We studied the pathogenesis of these lesions by examining the role of changes in specific glomerular capillary wall permeability properties in uninephrectomized rats. The development of altered capillary permselectivity to macromolecules and loss of glomerular basement membrane anionic charge were measured by the dextran fractional clearance and ferritin tracer probe methods, respectively. In addition, the protective effect of dietary protein restriction and an angiotensin I-converting enzyme inhibitor (captopril) were studied in eight groups of male Sprague-Dawley rats. Four groups of rats underwent sham-nephrectomy or left nephrectomy and were fed an 8.5% protein diet (sham-nephrectomy and low protein, nephrectomy and low protein) or a 30% protein diet, respectively (sham-nephrectomy and high protein, nephrectomy a high protein). Four other groups of rats underwent sham-nephrectomy or left nephrectomy and were treated with captopril (50 mg/kg/day) while receiving a 8.5% protein diet (sham-nephrectomy, low protein and captopril, nephrectomy, low protein and captopril) or a 30% protein diet, respectively (sham-nephrectomy, high protein and captopril, nephrectomy, high protein and captopril). Rats were nephrectomized at 21 days of age and were functionally tested and sacrificed at 7 months of age. The nephrectomy and high protein rats had significantly greater proteinuria and higher fractional clearance of neutral dextrans in the 30 to 42 A range compared with that of sham-nephrectomy and high protein, nephrectomy and low protein, and nephrectomy, high protein and captopril rats. The nephrectomy and high protein rats also had a significantly lower labeling of the glomerular basement membrane with cationic ferritin tracer molecules compared with the nephrectomy and low protein and nephrectomy, high protein and captopril rats. Of the eight treatment groups, the nephrectomy and high protein rats had the most severe glomerular lesions. In general, nephrectomized rats fed low dietary protein and nephrectomized rats treated with captopril had significantly less proteinuria, glomerular lesions, and milder changes in the glomerular capillary wall porosity and glomerular basement membrane anionic charge.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Effects of dietary protein and captopril on glomerular permselectivity in rats with unilateral nephrectomy. 245

Morphologic studies were performed in a passive model of in situ immune complex glomerulonephritis in rats. The formation and fate of subepithelial immune complexes as well as the role of glomerular polyanion in the induction of disease were examined. Unilateral in situ immune complex glomerulonephritis was induced in rats by perfusion of cationised horse spleen ferritin (pI greater than 9.5) (400 micrograms/rat) into the left kidney followed by systemic injection of 0.2 ml (= 400 micrograms precipitating antibody) of sheep anti-ferritin antiserum 2 h later. This schedule induced glomerulonephritis with proteinuria (mean maximum 100 mg/24 h between the 5th and the 12th day). Rats were sacrificed at intervals between 1 h and 42 days after induction of glomerulonephritis, samples of renal tissue were examined by light, immunofluorescence and electron microscopy (including staining of anionic sites by polyethyleneimine). The lesion induced closely resembled that of membranous glomerulonephritis in man as massive subepithelial deposits were seen with very little cellular infiltration or proliferation. The antigen (ferritin) deposits were initially located subepithelially; from 2 weeks onwards intramembranous deposits in the thickened basement membrane were present, the apparent translocation being due to excessive newly synthesised basement membrane material which encloses the deposits. A loss of anionic sites in the lamina rara interna, lamina rara externa and on the epithelial cell surface coat preceded the development of proteinuria.
 ...
PMID:Ultrastructural studies in passive in situ immune complex glomerulonephritis. A rat model for membranous glomerulonephritis. 248 73

We have studied the influence of steric factors on the clinico-pathologic expression of immune complex-mediated glomerular diseases, utilizing ferritin as an exogenous antigen. The tracer was planted in the left kidney either in the subepithelial layer of the glomerular capillary wall or on the endothelium and lamina rara interna. Subepithelial immune complex formation resulted in non-inflammatory injury with heterologous and autologous proteinuric phases (115 +/- 16 mg/24 hrs on day 2; 183 +/- 16 mg/24 hrs on day 9) lasting four to five weeks. The glomerular filtration rate of the experimental left kidney was reduced by 19% at day 3, and was increased by 20% at day 12 over right kidney values. Immune complexes persisted for more than seven weeks in the lamina rara externa. In contrast, immune complex deposition on the endothelium and in the lamina rara interna led to acute transient anuria, with a 38% drop in glomerular filtration rate at one hour, massive platelet accumulation, followed by a strong inflammatory response. Proteinuria did not develop. Functional and structural integrity was restored within 24 hours, with complete clearing of immune deposits. We conclude that the distribution of exogenous antigens within the capillary wall determines the structural and functional expression of immune-mediated glomerular diseases.
 ...
PMID:Determinants of immune complex-mediated glomerulonephritis. 297 36

The effects of increasing two dietary polyunsaturated fatty acids, eicosapentaenoic and linoleic, on the glomerulonephritis induced by repeated injections of apoferritin in the mouse were studied. Urinary protein excretion was measured serially; serum creatinine, aortic and renal production of eicosanoids and kidney histology were measured at sacrifice at 8 weeks. Both high EPA and LA feedings were associated with lesser proteinuria, normalization of renal function and profound changes in the tissue production of prostaglandin and thromboxane, which may explain their protective effect in this model of renal disease.
 ...
PMID:Protective effect of polyunsaturated fatty acid supplementation in apoferritin induced murine glomerulonephritis. 301 61

In pharmacologic doses E series prostaglandins attenuate the development of immune complex nephritis. We studied the effect of the dietary prostaglandin precursor linoleic acid on murine apoferritin-induced immune complex glomerulonephritis. High, normal, or low linoleic acid diets were fed to mice for 4 weeks prior to and during the intraperitoneal apoferritin administration. A high linoleic acid diet feeding was associated with less proteinuria, less renal histologic damage, and prevented a rise in serum creatinine. We conclude that linoleic acid has a protective effect on the development of murine apoferritin-induced immune complex nephritis.
 ...
PMID:Effects of dietary linoleic acid enrichment on induction of immune complex nephritis in mice. 315 80

The role of the major histocompatibility complex in the development of apoferritin induced immune complex glomerulonephritis was studied in H-2 congenic B10 mice. The glomerular lesions varied strikingly among the three different strains studied. The B10 (H-2b) mice had minimal mesangial expansion or no lesions at all. The B10.BR (H-2k) mice had mesangial expansion and proliferative glomerulonephritis without crescents or interstitial mononuclear cell infiltration. In contrast, the B10.D2 (H-2d) mice had necrotizing glomerulonephritis with crescents and an interstitial mononuclear cell infiltrate. Immunofluorescence and electron microscopy demonstrated only minimal mesangial deposits in B10 (H-2b) mice, predominantly mesangial deposition in the B10.BR (H-2k) mice, and mesangial and subepithelial immune complex deposits in B10.D2 (H-2d) mice. These morphologic differences correlated with functional abnormalities. Only the B10.D2 (H-2d) mice developed proteinuria, hematuria, and elevated blood urea nitrogen. They also had the most elevated antiapoferritin IgG levels. These experiments demonstrate that differences in the pathologic lesions and susceptibility to immune complex glomerulonephritis can be seen in animals that differ only at the H-2 locus. This model will lend itself to the study of the mechanisms by which the major histocompatibility complex influences the development of immune complex glomerulonephritis.
 ...
PMID:The role of H-2 in apoferritin-induced murine immune complex glomerulonephritis. 337 15


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>