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Ex vivo physiological compression of human osteoarthritis cartilage modulates cellular and matrix components


Autoři: Paolo Dolzani aff001;  Elisa Assirelli aff001;  Lia Pulsatelli aff001;  Riccardo Meliconi aff002;  Erminia Mariani aff001;  Simona Neri aff001
Působiště autorů: Laboratorio di Immunoreumatologia e Rigenerazione Tissutale, IRCCS Istituto Ortopedico Rizzoli, Bologna, Italy aff001;  Unità di Medicina e Reumatologia, IRCCS Istituto Ortopedico Rizzoli, Bologna, Italy aff002;  Dipartimento di Scienze Biomediche e Neuromotorie, Università di Bologna, Bologna, Italy aff003;  Dipartimento di Scienze Mediche e Chirurgiche, Università di Bologna, Bologna, Italy aff004
Vyšlo v časopise: PLoS ONE 14(9)
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pone.0222947

Souhrn

Mechanical stimulation appears to play a key role in cartilage homeostasis maintenance, but it can also contribute to osteoarthritis (OA) pathogenesis. Accumulating evidence suggests that cartilage loading in the physiological range contributes to tissue integrity maintenance, whereas excessive or reduced loading have catabolic effects. However, how mechanical stimuli can regulate joint homeostasis is still not completely elucidated and few data are available on human cartilage. We aimed at investigating human OA cartilage response to ex vivo loading at physiological intensity. Cartilage explants from ten OA patients were subjected to ex vivo controlled compression, then recovered and used for gene and protein expression analysis of cartilage homeostasis markers. Compressed samples were compared to uncompressed ones in presence or without interleukin 1β (IL-1β) or interleukin 4 (IL-4). Cartilage explants compressed in combination with IL-4 treatment showed the best histological scores. Mechanical stimulation was able to significantly modify the expression of collagen type II (collagen 2), aggrecan, SOX9 transcription factor, cartilage oligomeric matrix protein (COMP), collagen degradation marker C2C and vascular endothelial growth factor (VEGF). Conversely, ADAMTS4 metallopeptidase, interleukin 4 receptor alpha (IL4Rα), chondroitin sulfate 846 epitope (CS846), procollagen type 2 C-propeptide (CPII) and glycosaminoglycans (GAG) appeared not modulated. Our data suggest that physiological compression of OA human cartilage modulates the inflammatory milieu by differently affecting the expression of components and homeostasis regulators of the cartilage extracellular matrix.

Klíčová slova:

Cartilage – Collagens – Compression – Extracellular matrix – Histology – Homeostasis – Osteoarthritis – Chondrocytes


Zdroje

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