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

Giant cell tumors of bone dissociated by collagenase digestion were found to be composed of four different cell types defined by morphology, growth in culture, and pattern of staining with monoclonal antibodies. Giant cells comprised an average of 0.8% of the cells recovered, with the remainder consisting of small stromal cells. Of the giant cells, 20-57% expressed Ia antigens, while all lacked IgG Fc receptors and five differentiation antigens associated with mature members of the monocyte-macrophage lineage (M phi S-1, M phi P-9, M phi P-15, M phi S-39, and 63d3). One antigen, M phi U-50, found on early monocytoid forms was expressed on Ia+ giant cells. 6-36% of the remaining stromal tumor cells formed a second subpopulation that assumed either a rounded or elongated shape in culture. These cells bore Ia antigens, IgG Fc receptors, and five antigens of the monocyte-macrophage lineage usually found on blood monocytes. However, these cells differed from monocytes or macrophages in that the antigen M phi R-17 generally found on tissue macrophages was absent, and the M phi U-50 antigen present on more primitive cells was well expressed. A very limited endocytic capacity was demonstrable. A third population of up to 24% of the tumor cells was defined by the presence of intense staining for Ia antigens but the absence of antigens of mature monocytes. A proportion of these cells expressed M phi U-50 and a minority had IgG Fc receptors. The two Ia(+) populations of stromal cells were not identifiable after 2 wk of culture, nor did tumor cells selected for the presence of Ia antigens proliferate in culture. A fourth population of cells lacked Ia and monocyte lineage antigens, but showed pronounced intracellular staining for acid phosphatase. These cells had a distinctive plump epitheloid to fibroblastoid morphology and were readily established in long-term culture where they gave rise to large multinuclear Ia(-) cells containing acid phosphatase. The possibility is discussed that the cell types of these tumors relate to various stages in the development of osteoclasts from precursors in the mononuclear phagocyte lineage.
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PMID:Delineation of four cell types comprising the giant cell tumor of bone. Expression of Ia and monocyte-macrophage lineage antigens. 657 16

Pigmented villonodular synovitis (PVNS) is an idiopathic proliferative synovial process composed of two predominant cell types: mononuclear histiocytic cells and giant cells. This lesion can be locally invasive and can result in bone cyst formation and late cartilage and bone loss. Because metalloproteinases have been implicated in the joint destruction occurring in inflammatory arthritis and in the ability of certain tumors to invade adjacent tissues, their presence in PVNS was determined. Synovial tissue samples were collected at surgical synovectomy from the knees of 10 patients with a prior histological diagnosis of PVNS. Pigmented villonodular synovitis synovium was examined for the presence of the metalloproteinases collagenase and stromelysin. Messenger RNA (mRNA) for collagenase and stromelysin was present in all patient samples, although in varying amounts. In situ hybridization studies on synovial tissue sections identified synovial lining cells as the predominant cells expressing these metalloproteinases. Occasional infiltrating mononuclear histiocytic cells also were producing metalloproteinase mRNA. Giant cells did not express mRNA for the metalloproteinases collagenase and stromelysin. These results suggest that collagenase and stromelysin may be among the mediators of cartilage and bone loss that can occur in PVNS.
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PMID:Expression of metalloproteinases in pigmented villonodular synovitis. 805 25

Maximally effective concentrations of vanadate (a phosphotyrosine phosphatase inhibitor) increase glucose transport in muscle less than maximal insulin stimulation. This might be due to vanadate-induced decreased intrinsic activity of GLUT4 accompanying GLUT4 translocation. Thus, the effect of vanadate (NaVO3) on glucose transporter (GLUT4) intrinsic activity (V(max) = intrinsic activity x [GLUT4 protein]) was studied in muscle plasma membrane giant vesicles. Giant vesicles (average diameter 7.6 microns) were produced by collagenase treatment of rat skeletal muscle. The vesicles were incubated for 1.5 h with concentrations of vanadate ranging from 3 to 40 mmol l-1 at 34 degrees C before being used for determination of glucose transport. The dose-response curve showed that vanadate decreased the specific D-glucose uptake by a maximum of 70% compared with a control preparation. The vanadate-induced decrease in glucose uptake was not due to a decrease in number of vesicles. To further verify the apparent vanadate-induced decrease in GLUT4 intrinsic activity, the kinetics of glucose transport were also examined. In the presence of 10 mmol l-1 vanadate the V(max) and K(m) were decreased (P < 0.05, n = 6) 55% and 60%, respectively, compared with control. The plasma membrane GLUT4 protein content was not changed in response to vanadate. It is concluded that vanadate decreased glucose transport per GLUT4 (intrinsic activity). This finding suggests that regulation of glucose transport in skeletal muscle can involve changes in GLUT4 intrinsic activity.
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PMID:Effect of vanadate on glucose transporter (GLUT4) intrinsic activity in skeletal muscle plasma membrane giant vesicles. 867 62