Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nephritogenic antigen that induces antiglomerular basement membrane antibody-induced glomerulonephritis (anti-GBM nephritis) in rats was isolated from collagenase-solubilized bovine renal basement membranes. Purification was achieved using antibody-coupled affinity columns which were originally used for the purification of trypsin-solubilized nephritogenic antigen (Sado et al. 1984a). The nephritogenic antigen was a heteropolymer composed of P2 (Mr 28 kDa) and P3 (Mr 30 kDa) polypeptides as monomers and their dimers in sodium-dodecyl-sulfate (SDS) polyacrylamide gel electrophoresis. The P3 polypeptide was considered to be the nephritogenic epitope, since a fraction composed of the P2 polypeptide alone was not nephritogenic. The properties of the nephritogenic epitope were the same as those of the Goodpasture epitope (M2*), which is a noncollagenous domain of the alpha 3 chain of type IV collagen (Butkowski et al. 1985; Saus et al. 1988), indicating that the nephritogenic antigen is the same as the Goodpasture antigen.
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PMID:Properties of bovine nephritogenic antigen that induces anti-GBM nephritis in rats and its similarity to the Goodpasture antigen. 172 95

Experimental autoimmune glomerulonephritis was induced in inbred WKY/NCrj rats and Wistar (closed colony) rats by a single injection of isologous or homologous soluble antigens from glomerular and tubular basement membranes. Glomerular and tubular basement membranes were trypsin digested and applied to an affinity column to which rabbit antibodies to bovine nephritogenic antigen had been coupled. The adsorbed fraction was nephritogenic when it was injected into rat footpads with Freund's complete adjuvant. Glomerulonephritis with long-lasting proteinuria and haematuria developed 2 to 3 weeks after the injection, and it was characterized histologically by endocapillary hypercellularity of mononuclear cells, capsular adhesion, sclerosis of capillary tufts, and crescent formation. Immunofluorescence study revealed the linear deposition of rat IgG along the glomerular basement membrane. Some rats with the nephritis had pulmonary hemorrhage. These results suggest that this experimental model is similar to the experimental glomerulonephritis induced in rats by bovine nephritogenic antigen, and to human anti-glomerular basement membrane antibody-induced glomerulonephritis including Goodpasture's syndrome.
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PMID:Experimental autoimmune glomerulonephritis in rats by soluble isologous or homologous antigens from glomerular and tubular basement membranes. 331 5

Components were solubilized from human glomerular basement membrane by digestion with collagenase and pepsin or by extraction with guanidine-HCl either directly or after previous digestion with the enzyme. The diverse preparations were used as antigens in the enzyme-linked immunosorbent assay (ELISA) of antibody titers in sera from patients with Goodpasture syndrome and patients with other forms of glomerulonephritis, that is, systemic lupus erythematosus, periarteritis nodosa, and IgA-related nephropathy. Patients with Goodpasture syndrome had high titers of IgG antibodies reacting most strongly with collagenase digests. The antigen(s) was only partly solubilized by guanidine-HCl extraction, was destroyed by pepsin digestion as well as reduction, and partly destroyed by trypsin digestion. The antigen(s) is most likely noncollagenous protein. Antibodies from patients with other forms of nephritis were directed primarily against antigens in guanidine-HCl extracts, while the antigen(s) was not solubilized by collagenase digestion. Pepsin digestion destroyed the antigen(s). The antibodies were of a different class, that is, the patients with systemic lupus erythematosus had IgG and IgA as well as IgM antibodies; the patients with periarteritis nodosa had IgM or IgG and IgA antibodies, while the patients with IgA-related nephritis had the highest recorded titers of IgA but also had IgG as well as IgM antibodies. None of the patients had antibodies directed against triple helical collagen. The antibody response in anti-GBM antibody-related nephritis, then, is different both with respect to antigen and antibody class and depends on the underlying disease syndrome.
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PMID:Antiglomerular basement membrane antibody: antibody specificity in different forms of glomerulonephritis. 613 25