Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antibodies to myeloperoxidase (MPO) are found in the sera of patients with microscopic polyarteritis and idiopathic crescentic glomerulonephritis. Their pathogenicity is unknown. Studies were carried out on the binding of MPO to cultured human umbilical vein endothelial cells and the recognition of endothelium-bound MPO by antibody to MPO. Endothelial cells were cultured from human umbilical veins. The binding of MPO to endothelial cells and its inhibition by poly-D-lysine was detected using a monoclonal antibody to MPO and direct staining with APAAP and also by an enzyme-linked immunoassay (ELISA). The binding of anti-MPO antibody in the sera of patients with microscopic polyarteritis to endothelium-coated MPO was detected by ELISA. MPO bound to endothelial cells both on direct staining and ELISA and this binding was inhibited by the polycation poly-D-lysine, suggesting that it was charge mediated. Binding of anti-MPO antibody in the sera of patients with microscopic polyarteritis to endothelium-coated MPO was significantly higher than the binding of sera from normal subjects (P = 0.04), patients with idiopathic glomerulonephritis (P = 0.0005), and patients with lupus nephritis (P = 0.009). MPO binds to cultured human umbilical vein endothelium probably by a charge mechanism, and can react with anti-MPO antibodies in the sera of patients with microscopic polyarteritis as well as with a mouse monoclonal anti-MPO antibody. This binding of anti-MPO antibody to MPO fixed to the endothelial cell surface provides a mechanism by which endothelial injury and inflammation might occur in microscopic polyarteritis.
Nephrol Dial Transplant 1992
PMID:Endothelium myeloperoxidase-antimyeloperoxidase interaction in vasculitis. 133 32

Circulating autoantibodies, namely c-ANCA, MPO-ANCA, anti-Goodpasture (anti-NC1), and anti-entactin antibodies were analysed in sera from 82 consecutive patients with crescentic involvement of more than 50% glomeruli in renal biopsy specimens. Sixty-eight (approximately 83%) patients possessed one or more of these autoantibodies. About two-thirds of all patients had ANCA (c-ANCA, MPO-ANCA or both). Most of the remaining positive patients had anti-NC1 antibodies. Very few patients had anti-entactin antibodies, thereby suggesting a poor association of these antibodies with extracapillary glomerulonephritis (ECGN). Thus two different categories of patients, one possessing ANCA and the other anti-NC1 antibodies, could be recognised. Patients with anti-NC1 antibodies were characterised by linear immune deposits along the glomerular basement membrane and the clinical outcome was invariably grim. On the other hand, despite no significant difference in renal morphology from patients with anti-NC1 antibodies, the disease in patients with ANCA, in general, had a milder course. Among patients with ANCA, those with c-ANCA mainly had systemic small-vessel vasculitis with widespread systemic manifestations, whereas most patients with renal restricted primary ECGN with non-linear immune deposits possessed MPO-ANCA. Furthermore, patients with c-ANCA had a more severe disease than those with MPO-ANCA. These observations indicate that a continuous spectrum of diseases exists between idiopathic small-vessel vasculitides and primary non-linear ECGN. Our study also demonstrates that the presence of auto-antibodies is a dominant feature of severe ECGN and that the type of immunological injury is more important than the extent of crescentic involvement of glomeruli in determining the course of illness in patients with ECGN.
Nephrol Dial Transplant 1991
PMID:Circulating autoantibodies in patients with extracapillary glomerulonephritis. 165 14

The effect of chondroitin sulphate (CS) on peritoneal fluid and solute transport was studied in rats undergoing peritoneal dialysis. In the presence of CS, net ultrafiltration increased, while absorption of glucose and horseradish peroxidase from the peritoneal cavity decreased. Albumin, used instead of CS, did not modify either fluid or solute transport. In in vitro experiments on isolated rabbit mesentery, CS decreased transmembrane water flow induced by hydrostatic pressure, and its effect was not fully reversed 60 minutes after "wash-out" of this glycosaminoglycan. We postulate that the polyanionic CS molecules are trapped in the peritoneal interstitium, thus decreasing its hydraulic conductivity and permeability, which in turn increases net fluid removal during peritoneal dialysis because of its slower absorption from the peritoneal cavity.
Perit Dial Int 1991
PMID:Effects of chondroitin sulphate on fluid and solute transport during peritoneal dialysis in rats. 175 3

Glomerulonephritis was induced in rats by daily intravenous cationised bovine serum albumin. The conjugate of horseradish peroxidase with poly-L-lysine was injected as a tracer of endocytosis by glomerular epithelial cells. The rats were sacrificed serially from 1 min to 24 h after the injection of the conjugate. The cytochemical localisation of peroxidase was observed by light- and electron-microscopy. Peroxidase was detectable in the GBM and immune deposits from 1 min after the injection but was cleared by 2 h. Cellular membrane staining by the conjugate and the membrane invaginations containing concentrated peroxidase were prominent adjacent to the subepithelial immune deposits. Peroxidase was initially localised intracellularly in membrane-bound vesicles adjacent to the subepithelial deposits. They subsequently moved towards the cell centre and became larger, some having the characteristics of lysosomes. Peroxidase activity significantly diminished within the cells by 16 h. The results show that glomerular epithelial-cell endocytosis in immune-complex glomerulonephritis is similar to that observed in the normal, but cellular membrane binding and invagination are more prominent adjacent to immune deposits. The trapping of the tracer in the deposits did not seem to alter its property of being taken up by the epithelial cells.
Nephrol Dial Transplant 1990
PMID:Glomerular epithelial-cell endocytosis of horseradish peroxidase-polylysine conjugate in immune-complex glomerulonephritis. 215 4

The authors studied the in vitro permeability of different fragments of the rabbit's peritoneum to urea, inulin, horseradish peroxidase, and ferritin. Parietal peritoneum has a lower permeability to middle and large molecules than visceral peritoneum. In addition the local anesthetic, bupivacaine had a different effect on the mesothelial permeability of visceral peritoneum than on that of parietal peritoneum.
Perit Dial Int 1989
PMID:Permeability of different parts of the peritoneal mesothelium to solutes: an in vitro study. 248

Activity of acid phosphatase (AP), beta-glucuronidase (GR), N-acetyl-beta-D-glucosaminidase (GZ), and peroxidase (P) was assessed using a semiquantitative cytochemical method in peritoneal macrophages of 30 patients with end-stage renal failure treated by intermittent peritoneal dialysis and of 30 control patients with normal renal function. The dialysed patients showed a significantly higher activity of GR and P at the beginning of the treatment as compared with the respective activities observed in the control group and a further significant rise of these activities after 4 months of dialysis. Activity of AP at the beginning of the treatment was insignificantly lower than in the control group and the difference became significant at the end of the investigated period. There was no significant difference between the dialysed patients and the control group in the activity of GZ assessed at the beginning of the dialytic treatment and after 4 months of dialysis. A significant decrease in that activity was, however, observed in the course of dialysis.
Perit Dial Int 1989
PMID:Changes in activity of selected lysosomal enzymes in peritoneal macrophages of renal failure patients on peritoneal dialysis. 256 1

Using an original technique permitting repeated plasma exchange in the rat, we have tested this therapeutic approach in animals actively immunised with horseradish peroxidase, and in rats with HgCl2-induced autoimmune glomerulonephritis. Plasma exchange effectively removes circulating IgG anti-horseradish peroxidase antibodies from the sera of immunised rats. When applied to the model of HgCl2-induced antiglomerular basement membrane glomerulonephritis in Brown-Norway rats, this technique is also remarkably effective. In these rats, proteinuria is abolished during the plasma exchange treatment period and no circulating antiglomerular basement membrane antibodies can be detected. These antibodies are, however, found in the ultrafiltrates of exchanged rats. Serum IgE, characteristically elevated in HgCl2-treated rats, is also markedly diminished in exchanged rats. Control rats treated with infusions of fresh frozen plasma or with heparin alone did not show any improvement in disease severity. These results suggest that plasma exchange alone can attenuate antiglomerular basement membrane nephritis in HgCl2-treated rats. This observation may be of relevance for the treatment of human antiglomerular-basement membrane-mediated glomerulonephritis.
Nephrol Dial Transplant 1988
PMID:Plasma exchange in a rat model of autoimmune glomerulonephritis. 314 Jan 25

To investigate whether patients with IgA nephropathy have an exaggerated serum IgA response to ubiquitous food antigens we measured serum IgA antibodies to gliadin, ovalbumin, bovine serum albumin (BSA), beta-lactoglobulin and casein in 120 patients and 53 normal controls, using ELISA. No significant differences were observed between patients and controls in serum IgA antibodies against each of the antigens tested. Moreover, no correlation was found between serum IgA antibodies and IgA-immune complexes (IgA CIC). However, nine patients but no controls had an association of two or more IgA antibodies to dietary antigens. Sixty-six per cent of these patients (vs 24% in the remaining population) had IgA CIC, suggesting a possible involvement of these antibodies in the constitution of IgA CIC. Analysis of sera by HPLC revealed that both monomeric and higher molecular forms of IgA antibodies were present, the latter being coincident with the peak of IgA CIC. Preincubation of sera with serial concentrations of the specific antigen decreased significantly IgA CIC, suggesting that in this subgroup of patients IgA antibodies to food antigens (mainly BSA) are involved in the formation of IgA CIC. BSA-containing IgA CIC were in fact demonstrated by ELISA using rabbit IgG anti-BSA coated plates and peroxidase-conjugated anti-human IgA. The role of these CIC in the pathogenesis of IgA nephropathy needs to be further elucidated.
Nephrol Dial Transplant 1988
PMID:Food antigens, IgA-immune complexes and IgA mesangial nephropathy. 314 15

In a prospective multicentre study on the clinical significance of ANCA in renal diseases, sera from 920 patients with rapidly progressive renal failure and/or renal disease in association with extrarenal signs suggestive of a systemic vasculitis were tested for the presence of ANCA by indirect immunofluorescence (IIF) and ELISA. 193 of 920 cases (20.9%) were positive by IIF and 180 (19.5%) by ELISA, using a 'crude' cytoplasmic extract as substrate. The sensitivity and specificity of IIF for 'pauci-immune' cresentic necrotizing GN (CNGN), in association or not with systemic vasculitis, was 87.5 and 95.6% respectively. The IIF pattern and antigen specificity (alpha granules and MPO) correlated well with the clinical features: a cANCA pattern (alpha granules) was associated with ENT involvement (probable Wegener's granulomatosis); a pANCA pattern (MPO) with 'idiopathic' CNGN and small-vessel vasculitis without respiratory tract disease (microscopic polyarteritis); patients with a pulmonary-renal syndrome had either c or pANCA in a similar proportion. Our study confirms a high sensitivity and specificity of ANCA for patients with CNGN. ANCA should be considered an important diagnostic test in patients with renal diseases, especially in the presence of rapidly progressive renal failure.
Nephrol Dial Transplant 1994
PMID:Diagnostic significance and antigen specificity of antineutrophil cytoplasmic antibodies in renal diseases. A prospective multicentre study. Italian Group of Renal Immunopathology. 752 6

We have studied the distribution of immunoreactive growth factors, by an avidin-biotin-peroxidase technique, throughout the course of progressive renal scarring in rats submitted to extensive renal ablation. Groups of rats (n = 6) were sacrificed at Days 7, 15, 21, 30, 90 and 150 following subtotal nephrectomy (SNx) by ligation and resection of the renal poles. During the early stages, when compensatory renal growth took place, increased renal immunostaining for insulin-like growth factor-I (IGF-I) and epidermal growth factor (EGF) was detected within the collecting ducts and distal tubules, respectively. As renal scarring became established by Days 90 and 150, these two growth factors were detected within the cells of damaged and vacuolated distal tubules. By contrast, a progressive increase immunostain for platelet-derived growth factor (PDGF)-AB was apparent within the glomeruli from Day 15 onward preceding the onset of glomerulosclerosis. A third staining pattern was apparent by Day 15 for transforming growth factor-beta (TGF-beta) and by Day 30 for IGF-I consisting of a perivascular and interstitial distribution coinciding with adventitial expansion and tubulo-interstitial fibrosis, respectively. A mosaic of growth factors is expressed within the kidneys of rats submitted to extensive renal ablation.
Nephrol Dial Transplant 1995
PMID:Subtotal nephrectomy: a mosaic of growth factors. 779 26


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