ArticleArthritis research & therapy2022
Elevation of α-1,3 fucosylation promotes the binding ability of TNFR1 to TNF-α and contributes to osteoarthritic cartilage destruction and apoptosis.
Article in Arthritis research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Pooled it
- Punicic acid alleviates osteoarthritis progression through miR-29a-3p-dependent inhibition of the MAP2K6/p38 MAPK pathway.In vitro cellular & developmental biology. Animal · 2026Article
- Regulated Cell Death Pathways in Chondrocytes During Septic Arthritis: Current Evidence and Future Perspectives.Journal of inflammation research · 2026Review
- Immunohistochemical Expression of TNFR1, IL-6, and TGF-β1 in the Synovial Tissue of Patients with Hip Osteoarthritis.Biomedicines · 2025Article
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Observation of the Effects of Infrapatellar Fat Pad Excision on the Inflammatory Progression of Knee Osteoarthritis in Mice.Journal of inflammation research · 2025Article
- Identification of aberrant α-2,3 sialylation of cartilage associated with osteonecrosis of the femoral head based on integrated multi-omics analyses.BBA advances · 2025Article
- Blockade of the Notch Pathway by Inhibition of Fucosylation Ameliorates Chondrocyte Inflammation and Extracellular Matrix Degradation.Journal of inflammation research · 2025Article
- Proteome-wide Mendelian randomization and functional studies uncover therapeutic targets for polycystic ovarian syndrome.American journal of human genetics · 2024Article
- Sugar-coated bullets: Unveiling the enigmatic mystery 'sweet arsenal' in osteoarthritis.Heliyon · 2024Review
- Deciphering the Synthetic and Refolding Strategy of a Cysteine-Rich Domain in the Tumor Necrosis Factor Receptor (TNF-R) for Racemic Crystallography Analysis and d-Peptide Ligand Discovery.ACS bio & med chem Au · 2024Article
- The role of apoptosis in the pathogenesis of osteoarthritis.International orthopaedics · 2023Review
- Characterization of aberrant glycosylation associated with osteoarthritis based on integrated glycomics methods.Arthritis research & therapy · 2023Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOsteoarthritis (OA) is the most common form of arthritis and is characterized by the degradation of articular cartilage and inflammation of the synovial membrane. Fucosylation is an important feature of protein N/O-glycosylation and is involved in a variety of pathological processes, including inflammation and cancer. However, whether fucosylation impacts the OA pathological process is unknown.
methodsTotal proteins were extracted from cartilage samples obtained from patients with OA (n = 11) and OA rabbit models at different time points (n = 12). OA-associated abnormal glycopatterns were evaluated by lectin microarrays and lectin blots. The expression of fucosyltransferases involved in the synthesis of α-1,3 fucosylation was assessed by semi-qPCR. The synthesis of α-1,3 fucosylation mediated by FUT10 was interrupted by the transfection of siRNA, and the effect of α-1,3 fucosylation on OA-associated events was assessed. Then, immunoprecipitation and lectin blotting were used to investigate the relationship between the α-1,3 fucosylation level of tumor necrosis factor receptor superfamily member 1A (TNFR1) and OA. Finally, a TNFR1 antibody microarray was fabricated to evaluate the effect of α-1,3 fucosylation on the ability of TNFR1 to bind to tumor necrosis factor-α (TNF-α).
resultsElevated α-1,3 fucosylation was observed in cartilage from OA patients, rabbit models, and chondrocytes induced by TNF-α (fold change> 2, p< 0.01). Our results and the GEO database indicated that the overexpression of FUT10 contributed to this alteration. Silencing the expression of FUT10 impaired the ability of TNFR1 to bind to TNF-α, impeded activation of the NF-κB and P38/JNK-MAPK pathways, and eventually retarded extracellular matrix (ECM) degradation, senescence, and apoptosis in chondrocytes exposed to TNF-α.
conclusionThe elevation of α-1,3 fucosylation is not only a characteristic of OA but also impacts the OA pathological process. Our work provides a new positive feedback loop of "inflammation conditions/TNF-α/FUT10/α-1,3 fucosylation of TNFR1/NF-κB and P38/JNK-MAPK pathways/proinflammatory processes" that contributes to ECM degradation and chondrocyte apoptosis.
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