Abnormal expression of key genes and proteins in the canonical Wnt/ß-catenin pathway of articular cartilage in a rat model of exercise-induced osteoarthritis.
Mol Med Rep
; 13(3): 1999-2006, 2016 Mar.
Article
en En
| MEDLINE
| ID: mdl-26794964
ABSTRACT
To investigate the molecular pathogenesis of the canonical Wnt/ß-catenin pathway in exercise-induced osteoarthritis (OA), 30 male healthy Sprague Dawley rats were divided into three groups (control, normal exerciseinduced OA and injured exerciseinduced OA groups) in order to establish the exerciseinduced OA rat model. The mRNA and protein expression levels of Runx2, BMP2, Ctnnb1, Sox9, collagen â
¡, Mmp13, Wnt3a and ßcatenin in chondrocytes were detected by reverse transcriptionquantitative polymerase chain reaction, western blotting and immunohistochemical staining. The mRNA levels of Runx2, BMP2 and Ctnnb1 were upregulated in the normal exerciseinduced OA and injured exerciseinduced OA groups; while Runx2 and BMP2 were upregulated in the injured exerciseinduced OA group when compared with the normal exerciseinduced OA group. The protein levels of Mmp13, Wnt3a and ßcatenin were increased and collagen â
¡ was reduced in the normal exerciseinduced OA and injured exerciseinduced OA groups. Ctnnb1, Wnt3a and ßcatenin, which are key genes and proteins in the canonical Wnt/ßcatenin pathway, were abnormally expressed in chondrocytes of the exerciseinduced OA rat model. Ctnnb1, ßcatenin and Wnt3a were suggested to participate in the pathogenesis of exerciseinduced OA by abnormally activating the Wnt/ßcatenin pathway during physical exercise due to excessive pressure. The results of the present study may provide an improved understanding of the pathogenesis of exercise-induced OA.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Osteoartritis
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Condicionamiento Físico Animal
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Cartílago Articular
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Regulación de la Expresión Génica
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Beta Catenina
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Vía de Señalización Wnt
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Año:
2016
Tipo del documento:
Article