Journal
MOLECULAR MEDICINE REPORTS
Volume 13, Issue 3, Pages 1999-2006Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.4798
Keywords
exercise-induced osteoarthritis; Wnt; -catenin pathway; rat model; molecular pathogenesis
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Funding
- Laboratory Animal Center of Xi'an Jiaotong University Health Science Center
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To investigate the molecular pathogenesis of the canonical Wnt/-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 -catenin in chon-drocytes 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 -catenin were increased and collagen II was reduced in the normal exercise-induced OA and injured exercise-induced OA groups. Ctnnb1, Wnt-3a and -catenin, which are key genes and proteins in the canonical Wnt/-catenin pathway, were abnormally expressed in chondrocytes of the exercise-induced OA rat model. Ctnnb1, -catenin and Wnt-3a were suggested to participate in the pathogenesis of exercise-induced OA by abnormally activating the Wnt/-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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