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Biol. Res ; 48: 1-8, 2015. ilus, graf, tab
Article in English | LILACS | ID: biblio-950828

ABSTRACT

BACKGROUND: 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.


Subject(s)
Humans , Animals , Male , Female , Adolescent , Middle Aged , Aged , Mice , Rats , Young Adult , Chemokine CCL2/metabolism , Chondrocytes/metabolism , Osteoarthritis, Knee/physiopathology , Receptors, CCR2/metabolism , Synovial Membrane/cytology , In Vitro Techniques , Enzyme-Linked Immunosorbent Assay , Rats, Sprague-Dawley , Apoptosis/physiology , Disease Progression , Chemokine CCL2/genetics , Matrix Metalloproteinase 3/metabolism , Chondrocytes/enzymology , Iodoacetic Acid , Reverse Transcriptase Polymerase Chain Reaction , Matrix Metalloproteinase 13/metabolism , Receptors, CCR2/antagonists & inhibitors , Receptors, CCR2/genetics , Fibroblasts/metabolism , Matrilin Proteins/metabolism , Mice, Inbred C57BL
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