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Suchschritt : FT=glucosamine AND FT=osteoarthritis
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2/344 von 416    DIMDI: MEDLINE (ME60) © NLM
ND: ME10343772
PMID: 10343772
LR: 20061115
CED: 19990614
DCO: 19990614
Autoren: Piperno M; Reboul P; Hellio le Graverand MP; Peschard M; Annefeld M; Richard M; Vignon E
Titel: Osteoarthritic cartilage fibrillation is associated with a decrease in chondrocyte adhesion to fibronectin.
Quelle: Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society; VOL: 6 (6); p. 393-9 /199811/
PM: Print
SU: IM
Sprache: English
CY: ENGLAND
JID: 9305697
ISSN: 1063-4584
Institution: Claude Bernard University, Centre Hospitalier Lyon Sud, Pierre Bénite, France.
DT: Journal Article; Research Support, Non-U.S. Gov't
Schlagwörter
CT: AGED; CA(2+)-CALMODULIN DEPENDENT PROTEIN KINASE/antagonists & inhibitors; CELL ADHESION/drug effects; CELLS, CULTURED; CHONDROCYTES/drug effects; CHONDROCYTES/metabolism; CHONDROCYTES/*pathology; COLLAGEN/metabolism; ENZYME INHIBITORS/pharmacology; FIBRONECTINS/*metabolism; GLUCOSAMINE/analogs & derivatives; GLUCOSAMINE/metabolism; HUMANS; MIDDLE AGED; OSTEOARTHRITIS/metabolism; OSTEOARTHRITIS/*pathology; PROTEIN KINASE C/antagonists & inhibitors; SPHINGOSINE/pharmacology; SULFONAMIDES/pharmacology
CTG: ALTE MENSCHEN; CA(2+)-CALMODULIN-ABHÄNGIGE PROTEINKINASE/Antagonisten & Inhibitoren; ZELLADHÄSION/Arzneimittelwirkungen; ZELLEN, KULTIVIERTE; CHONDROZYTEN/Arzneimittelwirkungen; CHONDROZYTEN/Stoffwechsel; CHONDROZYTEN/*Pathologie; KOLLAGEN/Stoffwechsel; ENZYMINHIBITOREN/Pharmakologie; FIBRONECTINE/*Stoffwechsel; GLUCOSAMIN/Analoge & Derivate; GLUCOSAMIN/Stoffwechsel; MENSCH; MENSCHEN IM MITTLEREN LEBENSALTER; OSTEOARTHROSE/Stoffwechsel; OSTEOARTHROSE/*Pathologie; PROTEIN-KINASE C/Antagonisten & Inhibitoren; SPHINGOSIN/Pharmakologie; SULFONAMIDE/Pharmakologie
TE: Enzyme Inhibitors; Fibronectins; Sulfonamides; Sphingosine/123-78-4; glucosamine 2-sulfate/22487-35-0; Glucosamine/3416-24-8; W 7/65595-90-6; Collagen/9007-34-5; Ca(2+)-Calmodulin Dependent Protein Kinase/E.C. 2.7.1.123; Protein Kinase C/E.C. 2.7.1.37
CR: 123-78-4; 22487-35-0; 3416-24-8; 65595-90-6; 9007-34-5; E.C. 2.7.1.123; E.C. 2.7.1.37
AB: OBJECTIVE: Cartilage destruction in osteoarthritis (OA) is generally accepted as a failed repair process. Cell adhesion is implicated in tissue repair. Therefore, adhesion of OA chondrocytes to extracellular matrix proteins was investigated. DESIGN: Using chondrocytes from human OA femoral head cartilage, adhesion to fibronectin and type II collagen of cells from distinct areas showing an intact cartilage surface or a fibrillated cartilage surface was studied. Modulation of chondrocyte adhesion by both protein kinase C (PKC) inhibitors and glucosamine sulfate (GS) was also investigated. RESULTS: A significant (P < 0.05) decrease in adhesion to fibronectin of chondrocytes from fibrillated cartilage, relative to those from grossly normal OA cartilage, was demonstrated. Adhesion to type II collagen was not modified by the chondrocyte origins (either from normal or fibrillated OA cartilage). Adhesion to fibronectin of cells from grossly intact cartilage was decreased by the addition of PKC and calmodulin-dependent kinase inhibitors, W7 and sphingosine, to the cell culture. Adhesion to fibronectin of chondrocytes from fibrillated cartilage was significantly (P < 0.05) increased after glucosamine sulfate treatment. CONCLUSION: Fibrillation of cartilage from OA femoral head is associated with a defective adhesion of chondrocytes to fibronectin. The process is suggested to be dependent of PKC and/or calmodulin-dependent kinases and potentially reversible. Conceivably, it could play a role in OA cartilage destruction.
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