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osteoarthritis/protease
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The role of alpha-1-protease inhibitor (A1PI) in the inhibition of protease activity in human knee osteoarthritis.
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Alpha-1-protease inhibitor (A1PI) is the most abundant serum protease inhibitor, exhibiting inhibition of proteases known to act in osteoarthritis (OA) and rheumatoid arthritis. We have previously purified and sequenced A1PI synthesized by human articular cartilage and demonstrated in vitro
Comparison of diclofenac with apigenin-glycosides rich Clinacanthus nutans extract for amending inflammation and catabolic protease regulations in osteoporotic-osteoarthritis rat model.
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Oral treatment with a Brachystemma calycinum D don plant extract reduces disease symptoms and the development of cartilage lesions in experimental dog osteoarthritis: inhibition of protease-activated receptor 2.
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OBJECTIVE
The aims of this study were to evaluate the effect of oral treatment with a whole plant extract of Brachystemma calycinum D don (BCD) on the development of osteoarthritic lesions and symptoms in the experimental dog anterior cruciate ligament (ACL) transection model and to document its
Epicatechin and scopoletin rich Morinda citrifolia (Noni) leaf extract supplementation, mitigated Osteoarthritis via anti-inflammatory, anti-oxidative, and anti-protease pathways.
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The scopoletin (coumarin) and epicatechin (flavonoid) rich Morinda citrifolia L. (MC) Noni leaves are non-toxic (unlike the fruits) and consumed as vegetables. The anti-osteoarthritis effects of the MC leaf extract against joint cartilage degradation and inflammation were investigated through
The serine protease inhibitor trappin-2 is present in cartilage and synovial fluid in osteoarthritis.
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OBJECTIVE
Trappins are small serine protease inhibitors bound to extracellular matrix (ECM) through the actions of transglutaminase (TGase) enzymes. Trappin-2 is present in many tissues and is upregulated at sites of injury. In osteoarthritis (OA), serine proteases contribute to articular cartilage
The role of proteases in the pathogenesis of osteoarthritis.
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It is proposed that the cartilage contains enzymes which are responsible for the degradation of the principle components of the matrix, the proteoglycan and collagen. Measurement of acid, lysosomal bound proteases, or neutral proteases shows increases in proportion to the severity of the disease.
Down-regulation of protease-activated receptor 2 ameliorated osteoarthritis in rats through regulation of MAPK/NF-kB signaling pathway in vivo and in vitro.
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Recently, protease-activated receptor 2 (PAR2) has been proved to be involved in the inflammatory response including osteoarthritis (OA). In this study, we found that PAR2 antagonist could remarkably improve the pathological condition of OA rats in vivo. In addition, we also found that PAR2
Depletion of protease-activated receptor 2 but not protease-activated receptor 1 may confer protection against osteoarthritis in mice through extracartilaginous mechanisms.
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OBJECTIVE
To explore the involvement of protease-activated receptor 1 (PAR-1) and PAR-2 in the pathologic processes of osteoarthritis (OA) and to identify the cells/tissues primarily affected by ablation of PAR-1 or PAR-2 in mice.
METHODS
OA was induced in the joints of wild-type (WT), PAR-1(+/+) ,
Quantification of protease activities in synovial fluid from rheumatoid and osteoarthritis cases: comparison with antioxidant and free radical damage markers.
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We have compared (using the same series of experimental samples) the levels of activity of a comprehensive range of cytoplasmic, lysosomal and matrix protease types, together with the levels of free radical-induced protein damage (determined as protein carbonyl derivative) in synovial fluid from
Joint immobilization prevents murine osteoarthritis and reveals the highly mechanosensitive nature of protease expression in vivo.
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OBJECTIVE
Mechanical joint loading is critical for the development of osteoarthritis (OA). Although once regarded as a disease of cartilage attrition, OA is now known to be controlled by the expression and activity of key proteases, such as ADAMTS-5, that drive matrix degradation. This study was
[Research progress on protease-activated receptor 2 in pathogenesis of osteoarthritis].
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UNASSIGNED
To review the research progress on protease-activated receptor 2 (PAR-2) in the pathogenesis of osteoarthritis (OA).
UNASSIGNED
The relevant literature about the mechanism of PAR-2 in the occurrence and development of OA in recent years was extensively reviewed and comprehensively
Correlation of protease-activated receptor-2 expression and synovitis in rheumatoid and osteoarthritis.
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Protease-activated receptor-2 (PAR-2) is known to be pro-inflammatory and increasing evidence points to an inflammatory component in osteoarthritis. This investigation examined the relationship between synovitis and PAR-2 expression, histological and immunohistochemical analysis being performed on
Protease-activated receptor 2: a novel pathogenic pathway in a murine model of osteoarthritis.
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OBJECTIVE
Osteoarthritis is a global clinical challenge for which no effective disease-modifying agents currently exist. This study identified protease-activated receptor 2 (PAR-2) as a novel pathogenic mechanism and potential therapeutic target in osteoarthritis.
METHODS
Experimental osteoarthritis
In vivo fluorescence reflectance imaging of protease activity in a mouse model of post-traumatic osteoarthritis.
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OBJECTIVE
Joint injuries initiate a surge of inflammatory cytokines and proteases that contribute to cartilage and subchondral bone degeneration. Detecting these early processes in animal models of post-traumatic osteoarthritis (PTOA) typically involves ex vivo analysis of blood serum or synovial
Characteristics of the protease activity in synovial fluid from patients with rheumatoid arthritis and osteoarthritis.
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OBJECTIVE
To clarify which proteases are specifically activated in the lesions of rheumatoid arthritis (RA) and osteoarthritis (OA).
METHODS
The activity levels of the serine proteases of the coagulation and fibrinolytic systems, and of elastase and collagenase as controls, in synovial fluid from 27
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