Calcium-phosphate complex increased during subchondral bone remodeling affects earlystage osteoarthritis
Autor: | Youn-Kwan Jung, Min-Su Han, Dae Won Moon, Sun Young Lee, Ji-Ae Jang, Gun Woo Kim, Seungwoo Han, Eun Ju Lee, Hye-Ri Park |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Cartilage Articular Male STAT3 Transcription Factor chemistry.chemical_element lcsh:Medicine Osteoarthritis Calcium Matrix metalloproteinase Article Bone remodeling Phosphates 03 medical and health sciences Mice 0302 clinical medicine Chondrocytes Matrix Metalloproteinase 13 medicine Animals lcsh:Science 030203 arthritis & rheumatology Calcium metabolism Mitogen-Activated Protein Kinase 1 Multidisciplinary Mitogen-Activated Protein Kinase 3 Chemistry Kinase Cartilage lcsh:R NF-kappa B Cell Differentiation medicine.disease Endocytosis Cell biology Mice Inbred C57BL Disease Models Animal 030104 developmental biology medicine.anatomical_structure lcsh:Q Matrix Metalloproteinase 3 Bone Remodeling Signal transduction Signal Transduction |
Zdroj: | Scientific Reports Scientific Reports, Vol 8, Iss 1, Pp 1-10 (2018) |
ISSN: | 2045-2322 |
Popis: | An activation of osteoclasts and subchondral bone remodeling is a major histologic feature of early-stage osteoarthritis (OA), which can be accompanied by an increase of calcium (Ca) and phosphate (Pi) level in the subchondral milieu. Considering articular cartilage gets most of nutrition from subchondral bone by diffusion, these micro-environmental changes in subchondral bone can affect the physiology of articular chondrocytes. Here, we have shown that Ca is increased and co-localized with Pi in articular cartilage of early-stage OA. The Ca-Pi complex increased the production of MMP-3 and MMP-13 in the hypertrophic chondrocytes, which was dependent on nuclear factor-kappa B (NF-kB), p38 and extracellular signal-regulated kinase (Erk) 1/2 mitogen-activated protein (MAP) kinase and Signal transducer and activator of transcription 3 (STAT3) signaling. The Ca-Pi complexes increased the expression of endocytosis markers, and the inhibition of the formation of the Ca-Pi complex ameliorated the Ca-Pi complex-mediated increases of MMPs expression in hypertrophic chondrocytes. Our data provide insight regarding the Ca-Pi complex as a potential catabolic mediator in the subchondral milieu and support the pathogenic role of subchondral bone in the early stages of cartilage degeneration. |
Databáze: | OpenAIRE |
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