ArticleArthritis research & therapy2021
WNT16 elevation induced cell senescence of osteoblasts in ankylosing spondylitis.
Article in Arthritis research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 12 citations in OpenAlex.
- The Role of Wnt Signaling in Age-Related Alveolar Bone Loss and Regeneration.Journal of periodontal research · 2026Review
- Genomic structural equation modeling decodes skeletal aging: novel loci discovery and multisystem genetic crosstalk.Journal of translational medicine · 2025Article
- New insights into the role of cellular senescence and rheumatic diseases.Frontiers in immunology · 2025Review
- Investigating Potential Biomarkers of Ankylosing Spondylitis: A Study on Mitochondrial and Senescence Pathways Using Machine Learning.Journal of inflammation research · 2025Article
- Extracellular PPM1A promotes mineralization of osteoblasts differentiation in ankylosing spondylitis via the FOXO1A-RUNX2 pathway.Journal of cellular and molecular medicine · 2023Article
- WNT16 primer.Differentiation; research in biological diversityArticle
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Authors and funding
8 authors at 6 institutions in 1 country.
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Abstract
backgroundWNT16 is critical for bone homeostasis, but the effect of WNT16 in ankylosing spondylitis (AS) is still unknown. Here, we investigated whether WNT16 influences bone formation and pathophysiological changes of AS in an in vitro model.
methodsThe bone tissue from the facet joints was obtained from seven disease control and seven AS patients. Primary osteoprogenitor cells of the facet joints were isolated using an outgrowth method. Isolated osteoprogenitor cells from both control and AS tissues were analyzed by microarray, RT-qPCR, immunoblotting, and immunohistochemistry. The bone-forming activity of osteoprogenitor cells was assessed by various in vitro assays. β-galactosidase staining and senescence-associated secretory phenotype (SASP) using RT-qPCR were used to assess cell senescence.
resultsIn microarray analysis, WNT16 expression was significantly elevated in AS osteoprogenitor cells compared to the control. We also validated that WNT16 expression was elevated in AS-osteoprogenitor cells and human AS-bone tissues. WNT16 treatment inhibited bone formation in AS-osteoprogenitor cells but not in the control. Intriguingly, AS-osteoprogenitor cells were stained markedly with β-galactosidase for cell senescence in WNT16 treatment. Furthermore, in an H
conclusionWNT16 is highly expressed in AS and WNT16 treatment facilitated cell senescence in AS-osteoprogenitor cells during osteoblast differentiation accompanied by suppression of bone formation. The identified role of WNT16 in AS could influence bone loss in AS patients.
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