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dc.creatorXu,Yuan-kun
dc.creatorKe,Yan
dc.creatorWang,Bin
dc.creatorLin,Jian-hao
dc.date2015-01-01
dc.date.accessioned2019-05-02T21:22:31Z
dc.date.available2019-05-02T21:22:31Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602015000100064
dc.identifier.urihttp://revistaschilenas.uchile.cl/handle/2250/82600
dc.descriptionBACKGROUND: Osteoarthritis (OA) is a common arthritic disease and multifactorial whole-joint disease. Interactions of chemokines and OA is inadequately documented RESULTS: In vivo and in vitro studies were conducted to investigate monocyte chemoattractant protein 1 (MCP-1) and receptor chemokine (C-C motif) receptor 2 (CCR2) in chondrocyte degradation and cartilage degeneration. Chondrocytes from 16 OA patients and 6 normal controls were involved in this study. After stimulation of MCP-1, the expression of MCP-1 and CCR2 increased significantly (P < 0.001) and the expression of MMP-13 also increased (P < 0.05). MCP-1 stimulation also induced (or enhanced) the apoptosis of OA chondrocytes (P < 0.05). Additionally, the degradation of cartilage matrix markers (metalloproteinase 3 and 13, MMP3 and MMP13) in the culture medium of normal chondrocytes was also assessed. Furthermore, intra-articular injection of MCP-1 in mouse knees induced cartilage degradation and the CCR2 antagonist did not impede cartilage destroy in rats knees of monosodium iodoacetate (MIA) model CONCLUSIONS: The results of this study demonstrate that the MCP-1-CCR2 ligand-receptor axis plays a special role in the initiation and progression of OA pathology. Patients with ambiguous etiology can gain some insight from the MCP-1-CCR2 ligand-receptor axis
dc.formattext/html
dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.1186/S40659-015-0057-0
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.48 2015
dc.subjectMCP-1
dc.subjectCCR2
dc.subjectOsteoarthritis
dc.subjectChondrocyte
dc.subjectRat
dc.subjectMouse
dc.titleThe role of MCP-1-CCR2 ligand-receptor axis in chondrocyte degradation and disease progress in knee osteoarthritis


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