Abstract
BackgroundCartilage destruction is the main characteristic of osteoarthritis (OA), and osteopontin (OPN) is elevated in OA articular cartilage; however, the reason for the increased OPN level is not determined. In addition, Wnt/β-catenin signaling participates in the progression of OA. The aim of the present study was to evaluate whether canonical Wnt signaling could regulate the expression of OPN in human chondrocytes in vitro.MethodsHuman chondrocytes were cultured in vitro, and we first assayed the mRNA levels of OPN and β-catenin in chondrocytes. Next, we performed transient transfection of TCF 4 shRNA into chondrocytes to inhibit TCF 4 expression and explore changes in the OPN level. Then, the Wnt/β-catenin signaling inhibitor Dickkopf-1 (Dkk-1) was incubated with chondrocytes, and we assayed the changes in β-catenin and OPN.ResultsOur results showed that the expression of both β-catenin and OPN was increased in OA chondrocytes, but there were no correlations between β-catenin and OPN expression. TCF4 shRNA downregulated the expression of TCF 4 and OPN in chondrocytes, while after treatment with rDKK-1 at a concentration of 400 ng/ml for 24 h, the mRNA and protein expression of both β-catenin and OPN was significantly decreased in chondrocytes.ConclusionsElevated OPN expression might be regulated by the β-catenin/TCF-4 pathway, and the Wnt/β-catenin inhibitor DKK1 could inhibit the expression of β-catenin and OPN in OA chondrocytes.
Highlights
Osteoarthritis (OA) is the leading reason for disability and mainly affects the elderly [1]
Overexpression of β-catenin and OPN mRNA in OA chondrocytes In the present study, we detected the mRNA levels of βcatenin and OPN between chondrocytes isolated from parts of the knee cartilage of OA and non-OA patients
The results showed that shRNA-1105 decreased T cell factor (TCF)-4 mRNA and protein expression more efficiently than the other two sequences (P < 0.05) (Fig. 3b, c); TCF4 shRNA-1105 was used in the following experiment
Summary
Osteoarthritis (OA) is the leading reason for disability and mainly affects the elderly [1]. A previous study indicated that the levels of OPN in plasma, synovial. Other studies confirmed that OPN could promote the production of MMP13 and activation of the NF-kappaB pathway by increasing the abundance of p65 and phosphorylated p65 and the translocation of the p65 protein from the cytoplasm to the nucleus in chondrocytes [11]. Until recently, the main reason for the increased expression of OPN in OA was undetermined. Cartilage destruction is the main characteristic of osteoarthritis (OA), and osteopontin (OPN) is elevated in OA articular cartilage; the reason for the increased OPN level is not determined. The aim of the present study was to evaluate whether canonical Wnt signaling could regulate the expression of OPN in human chondrocytes in vitro
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