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rheumatic diseases/protease
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Autoantibodies to calpastatin (an endogenous inhibitor for calcium-dependent neutral protease, calpain) in systemic rheumatic diseases.
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We identified an autoantibody that reacts with calpastatin [an inhibitor protein of the calcium-dependent neutral protease calpain (EC 3.4.22.17)]. In early immunoblot studies, sera from patients with rheumatoid arthritis (RA) recognized unidentified 60-, 45-, and 75-kDa proteins in HeLa cell
Rheumatic Disease: Protease-Activated Receptor-2 in Synovial Joint Pathobiology.
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Protease-activated receptor-2 (PAR2) is one member of a small family of transmembrane, G-protein-coupled receptors. These receptors are activated via cleavage of their N terminus by serine proteases (e.g., tryptase), unveiling an N terminus tethered ligand which binds to the second extracellular
Macrophage proteases and rheumatic diseases: regulation of plasminogen activator by thymus-derived lymphocytes.
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Macrophages in culture secrete a variety of products including neutral protease activities such as plasminogen activator(s) (P.A.), collagenase and elastase. These products are not made by unstimulated macrophages, but only after induction by inflammatory stimuli, phagocytosis and lymphokines.
Multifunctional role of proteases in rheumatic diseases.
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Effect of antirheumatic drugs on neutral protease from human leucocyte granules.
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The inhibitory effect of 38 antirheumatic and other agents on purified neutral protease from human polymorphonuclear leucocytes has been studied by determining the decrease in enzyme activity on Z-Ala-NPH as substrate. Analgesics, salicylates, cytostatic agents and steroids, as well as
Alpha 1-antitrypsin in acute anterior uveitis and rheumatic diseases.
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To test the pathogenetic role of the phenotype MZ of alpha 1-antitrypsin/alpha 1-protease inhibitor (PI) in acute anterior uveitis (AAU) and in different rheumatic diseases we examined 360 unrelated patients including 93 with AAU alone, 24 patients with AAU and ankylosing spondylitis (AS), 21
[Value and significance of the immunologic determination of various serum sialoglycoproteins in rheumatic diseases of inflammatory nature].
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A statistical method was used in the evaluation of alpha-1-antitrypsin, acid alpha-1-glycoprotein, and haptoglobin in patients with rheumatic fever, rheumatoid arthritis, gout, periarthritis, arthrosis with inflammation, and primary arthrosis. A highly significant increase was noted in rheumatic
Characterization of specific proteases associated with the surface of human skin fibroblasts, and their modulation in pathology.
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Human skin fibroblasts were probed for cell surface protease activity. One activity removing dipeptides from the NH2-terminal end of Gly-Pro-pNA was specifically inhibited by di-isopropyl-fluorophosphate (DFP), phenylmethanesulphony fluoride (PMSF), and diprotin A, and thus was identified as
Quantitation and distribution of vitronectin in synovial fluid and tissue of patients with rheumatic disease.
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OBJECTIVE
Our study was undertaken to determine the quantity and pattern of distribution of vitronectin (Vn) in the synovial fluid and tissue of patients with rheumatic disease.
METHODS
We quantitated synovial fluid Vn levels in 37 patients (17 with rheumatoid arthritis (RA), 12 with crystal induced
Comparative assessment of vascular function in autoimmune rheumatic diseases: considerations of prevention and treatment.
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Numerous autoimmune-inflammatory rheumatic diseases have been associated with accelerated atherosclerosis or other types of vasculopathy leading to increased cardio- and cerebrovascular disease risk. Traditional risk factors, as well as the role of systemic inflammation including cytokines,
Alphavirus protease inhibitors from natural sources: A homology modeling and molecular docking investigation.
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Alphaviruses such as Chikungunya virus (CHIKV), O'Nyong-Nyong virus (ONNV), Ross River virus (RRV), Eastern equine encephalitis virus (EEEV), Venezuelan equine encephalitis virus (VEEV), and Western equine encephalitis virus (WEEV), are mosquito-transmitted viruses that can cause fevers, rash, and
Nuclear magnetic resonance and mass spectrometric studies on the action of proteases on pig articular cartilage.
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Rheumatic diseases are accompanied by a progradient diminution of the cartilage layer. Unfortunately, degradation mechanisms (role of different enzymes and reactive oxygen species) are not yet understood. Since nuclear magnetic resonance (NMR) spectroscopy was often used for the investigation of
Recommendations for coronavirus infection in rheumatic diseases treated with biologic therapy.
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The Coronavirus-associated disease, that was first identified in 2019 in China (CoViD-19), is a pandemic caused by a bat-derived beta-coronavirus, named SARS-CoV2. It shares homology with SARS and MERS-CoV, responsible for past outbreaks in China and in Middle East. SARS-CoV2 spread from China where
Trimer and tetramer complexes containing C1 esterase inhibitor, C1r and C1s, in serum and synovial fluid of patients with rheumatic disease.
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During activation, the first component of complement C1q (C1r-C1s)2 is dissociated in conjunction with the formation of complexes containing C1 esterase inhibitor (C1-INH). Trimer complexes, with zymogen C1s associated with a firm C1-INH-C1r complex (C1-INH-C1r-C1s) can be distinguished from
New areas for therapeutic intervention in the treatment of rheumatic disease.
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Anti-rheumatic therapy has been targeted against the symptoms arising from chronic inflammation of the joint. This has resulted in the extensive use of non-steroidal anti-inflammatory drugs. It is now becoming apparent that these agents have no beneficial effect on disease progression. This mini
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