The potential functional role of NEK2 was revealed to be related to the WNT/β-catenin signaling pathway, and miR-138 was the putative regulator of NEK2. miR-138 expression was downregulated while expressions of NEK2 and β-catenin as well as the phosphorylation levels of β-catenin were upregulated in mice with OA.
Here, we validated that the expression of forkhead box protein C1 (FoxC1) and β-catenin was upregulated in OA synovial membranes and synovial fibroblasts (SFs).
This study suggests that silencing lncRNA HOTAIR and inhibited Wnt/β-catenin pathway decline synovial inflammation and synoviocyte proliferation and promote apoptosis in OA rats.
In conclusion, the results indicated that the miR‑195‑5p inhibitor served a protective role in OA by inhibiting chondrocyte apoptosis and inflammatory responses by regulating the Wnt/β‑catenin and NF‑κB signaling pathways.
<b>Methods:</b> We used polymerase chain reaction (PCR) method to identify the expression levels of Cyclin D1 and down-stream Wnt/β-catenin pathway-related genes in OA chondrocytes according to the grade of OA.
Collectively, our findings indicated that HOTAIR/miR-17-5p/FUT2 axis contributed to OA progression via wnt/β-catenin pathway, which might provide novel insights into the function of lncRNA-driven in OA.
To further understand the role of β-catenin in osteoarthritis (OA) development in temporomandibular joint (TMJ), we have generated β-catenin conditional activation mice (β-cat(ex3) <sup>Agc1CreER</sup> ) by breeding Agc1-CreER mice with β-catenin<sup>flox(ex3)/+</sup> mice.
Compared to control group, increasing levels of β-catenin and MMP-13 expression with reduction of miR-320 and COL2A1 expressions were observed in OA chondrocytes.
To the best of our knowledge, this study is the first to report that SPN decreases interleukin-1β-induced inflammation in rat chondrocytes by inhibiting the activation of the NF-κB and wnt/β-catenin pathways, and, thus, has therapeutic potential in the treatment of OA.
Given the similar expression and activation patterns of HMGB2 and β-catenin in articular cartilage, the loss of these pathways in the SZ of articular cartilage may lead to altered gene expression, cell death and OA-like pathogenesis.
β-catenin levels were significantly increased (<i>p</i> < 0.001) in OA chondrocytes at basal conditions and significantly reduced (<i>p</i> < 0.01) by HP.
The aim of the current study was to determine the effect of parathyroid hormone (PTH) 1‑34 on cartilage degeneration, and the association between PTH 1‑34 and factors associated with the Wnt/β‑catenin pathway following anterior cruciate ligament and medial meniscectomy‑induced osteoarthritis (OA) in rats.
Our study provides evidence of a previously unknown link between Fibulin-4 and the canonical Wnt/β-catenin pathway that may contribute to our understanding of the molecular mechanisms of OA.
We further demonstrated that β-catenin, a key Wnt signaling transducer, was highly expressed in the OA treated groups using immunofluorescence stain assay.