• Shen-Shen Liu, Pu Zhou, and Yanqiu Zhang.
• College of Physical Education, Langfang Teachers University, Langfang, Hebei 065000, P.R. China.
• Mol Med Rep. 2016 Mar 1; 13 (3): 1999-2006.

AbstractTo investigate the molecular pathogenesis of the canonical Wnt/β-catenin pathway in exercise-induced osteoarthritis (OA), 30 male healthy Sprague Dawley rats were divided into three groups (control, normal exercise‑induced OA and injured exercise‑induced OA groups) in order to establish the exercise‑induced OA rat model. The mRNA and protein expression levels of Runx‑2, BMP‑2, Ctnnb1, Sox‑9, collagen Ⅱ, Mmp‑13, Wnt‑3a and β‑catenin in chondrocytes were detected by reverse transcription‑quantitative polymerase chain reaction, western blotting and immunohistochemical staining. The mRNA levels of Runx‑2, BMP‑2 and Ctnnb1 were upregulated in the normal exercise‑induced OA and injured exercise‑induced OA groups; while Runx‑2 and BMP‑2 were upregulated in the injured exercise‑induced OA group when compared with the normal exercise‑induced OA group. The protein levels of Mmp‑13, Wnt‑3a and β‑catenin were increased and collagen Ⅱ was reduced in the normal exercise‑induced OA and injured exercise‑induced OA groups. Ctnnb1, Wnt‑3a and β‑catenin, which are key genes and proteins in the canonical Wnt/β‑catenin pathway, were abnormally expressed in chondrocytes of the exercise‑induced OA rat model. Ctnnb1, β‑catenin and Wnt‑3a were suggested to participate in the pathogenesis of exercise‑induced OA by abnormally activating the Wnt/β‑catenin 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.

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