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Post-traumatic osteoarthritis development is not modified by postnatal chondrocyte deletion of Ccn2.
Keenan, Craig M; Ramos-Mucci, Lorenzo; Kanakis, Ioannis; Milner, Peter I; Leask, Andrew; Abraham, David; Bou-Gharios, George; Poulet, Blandine.
Afiliación
  • Keenan CM; Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, William Henry Duncan Building, West Derby Street, Liverpool L7 8TX, UK.
  • Ramos-Mucci L; Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, William Henry Duncan Building, West Derby Street, Liverpool L7 8TX, UK.
  • Kanakis I; Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, William Henry Duncan Building, West Derby Street, Liverpool L7 8TX, UK.
  • Milner PI; Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, William Henry Duncan Building, West Derby Street, Liverpool L7 8TX, UK.
  • Leask A; College of Dentistry, University of Saskatchewan, Saskatoon, SK S7N 5E4, Canada.
  • Abraham D; Centre for Rheumatology and Connective Tissue Diseases, University College London, London NW3 2PF, UK.
  • Bou-Gharios G; Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, William Henry Duncan Building, West Derby Street, Liverpool L7 8TX, UK.
  • Poulet B; Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, William Henry Duncan Building, West Derby Street, Liverpool L7 8TX, UK b.poulet@liverpool.ac.uk.
Dis Model Mech ; 13(7)2020 07 14.
Article en En | MEDLINE | ID: mdl-32616521
CCN2 is a matricellular protein involved in several crucial biological processes. In particular, CCN2 is involved in cartilage development and in osteoarthritis. Ccn2 null mice exhibit a range of skeletal dysmorphisms, highlighting its importance in regulating matrix formation during development; however, its role in adult cartilage remains unclear. The aim of this study was to determine the role of CCN2 in postnatal chondrocytes in models of post-traumatic osteoarthritis (PTOA). Ccn2 deletion was induced in articular chondrocytes of male transgenic mice at 8 weeks of age. PTOA was induced in knees either surgically or non-invasively by repetitive mechanical loading at 10 weeks of age. Knee joints were harvested, scanned with micro-computed tomography and processed for histology. Sections were stained with Toluidine Blue and scored using the Osteoarthritis Research Society International (OARSI) grading system. In the non-invasive model, cartilage lesions were present in the lateral femur, but no significant differences were observed between wild-type (WT) and Ccn2 knockout (KO) mice 6 weeks post-loading. In the surgical model, severe cartilage degeneration was observed in the medial compartments, but no significant differences were observed between WT and Ccn2 KO mice at 2, 4 and 8 weeks post-surgery. We conclude that Ccn2 deletion in chondrocytes does not modify the development of PTOA in mice, suggesting that chondrocyte expression of CCN2 in adults is not a crucial factor in protecting cartilage from the degeneration associated with PTOA.This article has an associated First Person interview with the first author of the paper.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoartritis / Cartílago Articular / Condrocitos / Factor de Crecimiento del Tejido Conjuntivo Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Dis Model Mech Asunto de la revista: MEDICINA Año: 2020 Tipo del documento: Article Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoartritis / Cartílago Articular / Condrocitos / Factor de Crecimiento del Tejido Conjuntivo Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Dis Model Mech Asunto de la revista: MEDICINA Año: 2020 Tipo del documento: Article Pais de publicación: Reino Unido