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Glucosamine promotes chondrocyte proliferation via the Wnt/β-catenin signaling pathway

The present study investigated the mechanism underlying the effects of glucosamine (GlcN) on the proliferation of chondrocytes isolated from the knee cartilage of Sprague-Dawley rats. Chondrocytes were treated with various concentrations of GlcN or without GlcN. The effects of GlcN on chondrocyte pr...

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Detalles Bibliográficos
Autores principales: Ma, Yuhuan, Zheng, Wenwei, Chen, Houhuang, Shao, Xiang, Lin, Pingdong, Liu, Xianxiang, Li, Xihai, Ye, Hongzhi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5979785/
https://www.ncbi.nlm.nih.gov/pubmed/29568900
http://dx.doi.org/10.3892/ijmm.2018.3587
Descripción
Sumario:The present study investigated the mechanism underlying the effects of glucosamine (GlcN) on the proliferation of chondrocytes isolated from the knee cartilage of Sprague-Dawley rats. Chondrocytes were treated with various concentrations of GlcN or without GlcN. The effects of GlcN on chondrocyte proliferation were determined using reverse transcription-polymerase chain reaction, western blot analysis and immunohistochemistry. The results indicated that GlcN significantly improved chondrocyte viability, accelerated G(1)/S transition during progression of the cell cycle and promoted the expression of cell cycle regulatory proteins, including cyclin D1, cyclin-dependent kinase (CDK)4 and CDK6, thus indicating that GlcN may promote chondrocyte proliferation. Furthermore, GlcN upregulated the expression levels of Wnt-4, Frizzled-2 and β-catenin, and downregulated the expression of glycogen synthase kinase-3. GlcN also promoted β-catenin translocation; β-catenin is able to activate numerous downstream target genes, including cyclin D1. To determine the role of the Wnt/β-catenin signaling pathway in chondrocyte proliferation, the Wnt/β-catenin signaling pathway was inhibited using Dickkopf-1 (DKK-1), after which chondrocytes were treated with GlcN. The results demonstrated that the expression levels of β-catenin and cyclin D1 were decreased in chondrocytes treated with DKK-1 and GlcN. These results suggested that GlcN may promote chondrocyte proliferation via the Wnt/β-catenin signaling pathway.