ArticleJournal of orthopaedic surgery and research2021
Silencing of Vangl2 attenuates the inflammation promoted by Wnt5a via MAPK and NF-κB pathway in chondrocytes.
Article in Journal of orthopaedic surgery and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Promoter Methylation of WIF1 is Involved in IL-17-Induced Chondrocyte Inflammatory Injury and Matrix Degradation via Promoting Wnt5a/MAPK-JNK Signaling.Molecular biotechnology · 2026Article
- Intra-articular delivery of Si-Vangl2 limits cartilage degeneration in an osteoarthritis rat model.Frontiers in bioengineering and biotechnology · 2026Article
- Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulations to Elucidate the Potential Mechanism of Ermiao San in Osteoarthritis.Food science & nutrition · 2025Article
- The mechanism of curcumin protecting against IL-1β-induced oxidative stress and inflammation in chondrocytes via the Bmp2/Smad5/Runx2 pathway.Cytotechnology · 2025Article
- From polarity to pathology: Decoding the role of cell orientation in osteoarthritis.Journal of orthopaedic translation · 2024Review
- Stearoylation cycle regulates the cell surface distribution of the PCP protein Vangl2.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Small interfering RNAs in the management of human osteoporosis.British medical bulletin · 2023Review
- Identification and validation of key long non-coding RNAs in resveratrol protect against IL-1β-treated chondrocytes via integrated bioinformatic analysis.Journal of orthopaedic surgery and research · 2021Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe Wnt planar cell polarity (PCP) pathway is implicated in osteoarthritis (OA) both in animals and in humans. Van Gogh-like 2 (Vangl2) is a key PCP protein that is required for the orientation and alignment of chondrocytes in the growth plate. However, its functional roles in OA still remain undefined. Here, we explored the effects of Vangl2 on OA chondrocyte in vitro and further elucidated the molecular mechanism of silencing Vangl2 in Wnt5a-overexpressing OA chondrocytes.
methodsChondrocytes were treated with IL-1β (10 ng/mL) to simulate the inflammatory microenvironment of OA. The expression levels of Vangl2, Wnt5a, MMPs, and related proinflammatory cytokines were measured by RT-qPCR. Small interfering RNA (siRNA) of Vangl2 and the plasmid targeting Wnt5a were constructed and transfected into ATDC5 cells. Then, the functional roles of silencing Vangl2 in the OA chondrocytes were investigated by Western blotting, RT-qPCR, and immunocytochemistry (ICC). Transfected OA chondrocytes were subjected to Western blotting to analyze the relationship between Vangl2 and related signaling pathways.
resultsIL-1β induced the production of Vangl2, Wnt5a, and MMPs in a time-dependent manner and the significantly increased expression of Vangl2. Vangl2 silencing effectively suppressed the expression of MMP3, MMP9, MMP13, and IL-6 at both gene and protein levels and upregulated the expression of type II collagen and aggrecan. Moreover, knockdown of Vangl2 inhibited the phosphorylation of MAPK signaling molecules (P38, ERK, and JNK) and P65 in Wnt5a-overexpressing OA chondrocytes.
conclusionsFor the first time, we demonstrate that Vangl2 is involved in the OA process. Vangl2 silencing can notably alleviate OA progression in vitro by inhibiting the expression of MMPs and increasing the formation of the cartilage matrix and can inhibit the proinflammatory effects of Wnt5a via MAPK and NF-κB pathway. This study provides new insight into the mechanism of cartilage inflammation.
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