Dokumente
Suchschritt : FT=glucosamine AND FT=osteoarthritis
» Fenster schließen »

2/64 von 416 DIMDI: MEDLINE (ME60) © NLM

ND: | ME16300972
PMID: | 16300972
LR: | 20061115
CED: | 20060313
DCO: | 20060503
Autoren: | Uitterlinden EJ; Jahr H; Koevoet JL; Jenniskens YM; Bierma-Zeinstra SM; Degroot J; Verhaar JA; Weinans H; van Osch GJ
Titel: | Glucosamine decreases expression of anabolic and catabolic genes in human osteoarthritic cartilage explants.
Quelle: | Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society; VOL: 14 (3); p. 250-7 /200603/
PM: | Print-Electronic
EPD: | 20051118
SU: | IM
Sprache: | English
CY: | England
JID: | 9305697
ISSN: | 1063-4584
Institution: | Erasmus MC, University Medical Center Rotterdam, Department of Orthopaedics, The Netherlands.
DT: | Journal Article
Schlagwörter
CT: | AGED; AGGRECANS; CARTILAGE, ARTICULAR/*drug effects; CARTILAGE, ARTICULAR/metabolism; COLLAGEN TYPE II/biosynthesis; COLLAGEN TYPE II/genetics; DOWN-REGULATION/*drug effects; EXTRACELLULAR MATRIX PROTEINS/biosynthesis; EXTRACELLULAR MATRIX PROTEINS/genetics; GLUCOSAMINE/*pharmacology; HUMANS; LECTINS, C-TYPE/biosynthesis; LECTINS, C-TYPE/genetics; MATRIX METALLOPROTEINASES/biosynthesis; MATRIX METALLOPROTEINASES/genetics; MIDDLE AGED; OSTEOARTHRITIS, KNEE/*metabolism; OSTEOARTHRITIS, KNEE/pathology; PROTEOCHONDROITIN SULFATES/biosynthesis; PROTEOCHONDROITIN SULFATES/genetics; TISSUE CULTURE TECHNIQUES; TISSUE INHIBITOR OF METALLOPROTEINASES/biosynthesis; TISSUE INHIBITOR OF METALLOPROTEINASES/genetics
CTG: | ALTE MENSCHEN; AGGREKANE; KNORPEL, GELENK-/*Arzneimittelwirkungen; KNORPEL, GELENK-/Stoffwechsel; KOLLAGEN TYP II/Biosynthese; KOLLAGEN TYP II/Genetik; DOWN-REGULATION/*Arzneimittelwirkungen; EXTRAZELLULÄRE MATRIXPROTEINE/Biosynthese; EXTRAZELLULÄRE MATRIXPROTEINE/Genetik; GLUCOSAMIN/*Pharmakologie; MENSCH; LECTINE, C-TYP-/Biosynthese; LECTINE, C-TYP-/Genetik; MATRIX-METALLOPROTEINASEN/Biosynthese; MATRIX-METALLOPROTEINASEN/Genetik; MENSCHEN IM MITTLEREN LEBENSALTER; OSTEOARTHROSE, KNIE/*Stoffwechsel; OSTEOARTHROSE, KNIE/Pathologie; PROTEOCHONDROITIN-SULFATE/Biosynthese; PROTEOCHONDROITIN-SULFATE/Genetik; GEWEBEKULTUREN, TECHNIKEN FÜR; GEWEBSINHIBITOREN VON METALLOPROTEINASEN/Biosynthese; GEWEBSINHIBITOREN VON METALLOPROTEINASEN/Genetik
TE: | Aggrecans; Collagen Type II; Extracellular Matrix Proteins; Lectins, C-Type; Proteochondroitin Sulfates; Tissue Inhibitor of Metalloproteinases; Glucosamine/3416-24-8; Matrix Metalloproteinases/E.C. 3.4.24.-
CR: | 3416-24-8; E.C. 3.4.24.-
AB: | OBJECTIVE: To investigate the effect of glucosamine (GlcN) in a human osteoarthritic explant model on expression of genes involved in anabolic and catabolic activities of chondrocytes. METHODS: Human osteoarthritic explants, obtained during knee arthroplasty surgery, were pre-cultured (3 days) and treated with glucosamine-hydrochloride (GlcN-HCl) or glucosamine-3-sulphate (GlcN-S) at 0.5mM and 5mM (4 days). RNA was isolated from the explants and real time RT-PCR was performed. Additionally, total matrix metalloproteinase (MMP) activity was measured in culture medium. RESULTS: Addition of 5mM GlcN led to significant down-regulation of aggrecan (2.65-7.73-fold) and collagen type II (7.75-22.17-fold) gene expression, indicating inhibited anabolic activity. Considering catabolic activities, 5mM GlcN significantly down-regulated aggrecanase-1 and MMP3 and 5mM GlcN-S additionally down-regulated aggrecanase-2 and tissue inhibitor of MMP gene expression significantly. Gene expression was not significantly altered by 0.5mM GlcN. Total MMP activity in culture medium was only significantly reduced after addition of 5mM GlcN-HCl. CONCLUSION: The effects of GlcN on gene expression in a human osteoarthritic explant model suggest that enzymatic breakdown of the extra-cellular matrix might be reduced by the addition of 5mM GlcN. Additionally, restoration of already damaged cartilage is not to be expected, because gene expression of anabolic genes is also down-regulated. We suggest that chondroprotective properties of GlcN in vivo may be based on inhibiting further degradation due to catabolic activities, rather than on the ability to rebuild cartilage.

» Volltext »
» Fenster schließen »