Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The effects of intravenous administration of pepsin on autologous immune complex glomerulonephritis, which is an established experimental model of membranous glomerulopathy in human, were investigated. Sensitization of rats with renal tubular antigen induced an increase in urinary protein excretion, decreases in serum levels of total protein, albumin and immunoglobulin G and histopathological abnormalities in glomerulus. A significant increase in serum immune complex and glomerular immune complex deposit were also observed. These abnormalities were ameliorated by pepsin. Pepsin may be effective and beneficial in the treatment of immune complex nephritis.
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PMID:The effect of pepsin on autologous immune complex glomerulonephritis. 622 64

The effects of pepsin on autoimmune glomerulonephritis of MRL/1 mice were investigated. Intravenous administration of pepsin significantly improved survival rate and suppressed progressive increase in urinary excretion of protein and various histopathological changes in kidney. Increased serum levels of immune complex and anti-DNA antibody in MRL/1 mice were decreased by pepsin. Pepsin ameliorated abnormalities in lymphocyte subsets and lymphocyte functions. The fact that pepsin ameliorated abnormalities in immune function may contribute to the preventive effects of pepsin against pathogenesis and progress of immune complex nephritis.
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PMID:Pepsin and autoimmune disease mouse. 641 57

The effects of pepsin on autoimmune glomerulonephritis of New Zealand Black and White F1 hybrid (NZB/W F1) mice were investigated. Intravenous pepsin significantly improved survival rate and suppressed progressive increase in urinary protein and histopathological changes in kidney. Increased serum levels of immune complexes, anti-DNA antibody and natural thymocytotoxic autoantibody were decreased and abnormalities in lymphocyte subsets were ameliorated by pepsin. Pepsin suppressed autoantibody production and enhanced antibody production against xenogeneic substance in these mice. The fact that pepsin ameliorates abnormalities in immune function may contribute to the preventive effects of pepsin against pathogenesis and progression of immune complex nephritis.
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PMID:The effects of pepsin on the natural progression of autoimmunity in glomerulonephritis in the NZB/W F1 mouse. 643 24