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Dishevelled-2 modulates osteogenic differentiation of human synovial fibroblasts in osteoarthritis
Dishevelled (Dvl)-2 represents one of the cytoplasmic proteins, which serves as a pivotal hub in signaling intermediates through a number of different signaling pathways associated with the Wnt family. The aim of the present study was to investigate the roles and mechanisms of Dvl-2 on synovial fibr...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059681/ https://www.ncbi.nlm.nih.gov/pubmed/29749449 http://dx.doi.org/10.3892/mmr.2018.8975 |
Sumario: | Dishevelled (Dvl)-2 represents one of the cytoplasmic proteins, which serves as a pivotal hub in signaling intermediates through a number of different signaling pathways associated with the Wnt family. The aim of the present study was to investigate the roles and mechanisms of Dvl-2 on synovial fibroblasts (SFBs) in osteoarthritis (OA). A Cell Counting kit-8 (CCK-8) assay was used to determine cell viability. An alkaline phosphatase (ALP) test kit was used to measure the activity of ALP. Western blot and reverse transcription-quantitative polymerase chain reaction analysis were used to evaluate the protein and mRNA expression, respectively. The results suggest that depletion of Dvl-2 significantly decreased the expression of osteoprotegerin (OPG) and ALP (P<0.05) and significantly increased the expression of receptor activator of nuclear factor-κB ligand (RANKL), ALP, osteonectin (ON), osteocalcin (OCN) and osterix (P<0.05). In addition, the depletion of Dvl-2 also significantly inhibited the expression of runt-related transcription factor 2 (Runx-2) and β-catenin in SFBs (P<0.05). The effect of Dvl-2 over-expression was opposite to the effect of Dvl-2 silencing. The inactivation of Wnt3a reversed the effect of Dvl-2 silencing. In conclusion, the results indicate that Dvl-2 regulated osteogenic differentiation of SFBs in OA. |
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