Glucosamine Promotes Chondrocyte Proliferation Via The Wnt/Beta-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 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 beta-catenin, and downregulated the expression of glycogen synthase kinase-3. GlcN also promoted beta-catenin translocation; beta-catenin is able to activate numerous downstream target genes, including cyclin D1. To determine the role of the Wnt/beta-catenin signaling pathway in chondrocyte proliferation, the Wnt/beta-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 beta-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/beta-catenin signaling pathway.