ArticleMolecular medicine reports2018
Dishevelled‑2 modulates osteogenic differentiation of human synovial fibroblasts in osteoarthritis.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Silver nanoparticles promote osteogenic differentiation of mouse embryonic fibroblastsAmerican journal of stem cells · 2023Article
- High-throughput sequencing analysis of the expression profile of microRNAs and target genes in mechanical force-induced osteoblastic/cementoblastic differentiation of human periodontal ligament cells.American journal of translational research · 2019Article
- MicroRNA-29a-3p enhances dental implant osseointegration of hyperlipidemic rats via suppressing dishevelled 2 and frizzled 4.Cell & bioscience · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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