Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leukocyte adherence inhibition (LAI) test was examined in 35 patients with renal diseases and 14 normal controls, using collagenase-treated glomerular basement membrane, glycosidase-treated glomerular basement membrane and renal tubular epithelium as antigens. Although the control group showed strikingly similar mean LAI indices for all antigens tested, the whole group of patients with renal diseases showed a wide scatter of values. Two categories of patients had significantly increased LAI indices (p less than 0.01) when their mean values were compared with those of normal controls: (1) rapidly progressive glomerulonephritis (RPGN) and (2) lupus nephritis (SLE). In the serial studies of the RPGN and SLE cases, there were no significant changes in the pattern of LAI and they continued to give positive and very comparable results when re-examined at intervals of 1-6 months. Out of the 30 patients who were able to be evaluated with the three antigens, 15 cases exhibited positive LAI response to two or more antigens simultaneously. These in vitro findings suggest that there is an abnormal cellular response to certain antigen or widespread LAI reactivity to a variety of renal antigens in certain forms of human glomerulonephritis.
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PMID:Leukocyte adherence inhibition test in renal diseases. 617 83

The identity of many endothelial cell autoantigens remains unclear. This study has used human monoclonal anti-endothelial cell autoantibodies isolated from patients with SLE to identify endothelial autoantigens. Thirteen antibodies reactive with endothelial cell membrane preparations were isolated and cloned, one of which has previously been demonstrated to be pro-inflammatory. Western blotting demonstrates that these antibodies recognize a variety of proteins in endothelial cell membrane preparations. Further characterization of five antibodies by cDNA library screening, immunofluorescence and Western blotting proves that two of these antibodies recognized the cytoskeletal proteins tubulin and vimentin. A further antibody identified a clone derived from human collagenase, an identification supported by Western blotting. The multiple clones selected by other antibodies are not compatible with the molecular weight of the antigen recognized in Western blotting studies. This study has clearly identified two endothelial cell autoantigens present in membrane preparations and provides strong evidence as to the identity of a third.
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PMID:The identification of endothelial cell autoantigens. 1093 27

Immune imbalance in SLE increases the susceptibility to infectious diseases. The aim of this study was to analyze several mechanisms related to non-specific immunity in this autoimmune disorder. We studied in vivo CD11b expression, phagocytosis, and chemotaxis in polymorphonuclear cells (PMN) from SLE patients. All tests were also performed under hrIL-8 stimulating conditions and analyzed by flow cytometry. Intracellular leucocyte (monocytes and PMN) enzyme activity was evaluated using specific substrates for cathepsin B and D, collagenase, and oxidative burst by flow cytoenzymology. An exaggerated in vivo CD11b expression was observed on PMN from SLE patients without noticeably in vitro effect upon hrIL-8. Similarly both, phagocytosis and chemotaxis were diminished and showed no response to hrIL-8 stimulation. The opposite was found in PMN from controls. Intracellular enzyme activity was comparable between groups as far as cathepsin B and D are concerned. A tendency of decreased oxidative-burst induction was noted in monocytes and PMN from SLE patients, whereas collagenase activity was found clearly increased in both leucocyte subpopulations. Our results may represent a deficient ability of the innate immune mechanisms for the clearance of infectious agents, immune complexes, satisfactory resolution of inflammatory processes and tissue repair in SLE.
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PMID:Innate immune mechanisms in the pathogenesis of systemic lupus erythematosus (SLE). 1141 Feb 51

We investigated the serum concentration of total metalloproteinase-9 (tMPP-9), active MMP-9 (aMMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) in a group of 41 patients with SLE and 20 healthy controls. Serum levels of tMMP-9 and TIMP-1 were assessed by an enzyme-linked immunosorbent assay (ELISA) and aMMP-9 by fluorometric assay. The tMMP-9 level was lower in SLE patients (mean 262 ng/mL) than in healthy volunteers (mean 325 ng/mL) (P = .048). Similarly, aMMP-9 level was lower in SLE patients (mean 121 ng/mL) than in control group (mean 169 ng/mL) (P = .0355) and lower in active SLE (mean 54 ng/mL) than in inactive disease (mean 99 ng/mL) (P = .033). TIMP-1 level was also lower in SLE patients (mean 181 ng/mL) than in control group (mean 233 ng/mL) (P = .004). In SLE patients, a positive correlation was found between tMMP-9 and aMMP-9 (rho = 0.568; P = .001). We also found a positive correlation of tMMP-9 and TIMP-1 with VEGF concentrations (rho = 0.450, P = .005 and rho = 0.387; P = .018, resp). tMMP-9, aMMP-9, and TIMP-1 serum levels are lower in SLE patients than in healthy control group.
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PMID:Circulating total and active metalloproteinase-9 and tissue inhibitor of metalloproteinases-1 in patients with systemic lupus erythomatosus. 1686 98