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Updated: Oct 16, 2026

Labeling of Extracellular Vesicles for Monitoring Migration and Uptake in Cartilage Explants
Published on: October 4, 2021
Synovial fluid-derived extracellular vesicles modulate joint cell function in osteoarthritis
Alvaro Compañ1, Vittoria Carrabs2, María Luisa Ferrándiz1,3
1Interuniversity Research Institute for Molecular Recognition and Technological Development (IDM), Universitat Politècnica de València, Universitat de València, Valencia, Spain.
Introduction:
Osteoarthritis (OA) is an age-related joint disease characterized by chronic inflammation and extracellular matrix degradation. Extracellular vesicles (EVs) in synovial fluid (SF) may modulate intercellular communication and influence disease progression.
Material And Methods:
SF, cartilage, and synovial tissue were collected from knee OA patients (n = 68). SF-derived EVs (SF-EVs) were isolated by size exclusion chromatography and characterized by transmission electron microscopy (TEM), tunable resistive pulse sensing (qNano), and ELISA analysis of EV-associated markers (CD9, CD81, TSG101, and PDCD6IP) and the negative marker calnexin. In vitro experiments were performed using primary synoviocytes and chondrocytes stimulated with interleukin (IL)-1β in the presence or absence of SF-EVs. Inflammatory and catabolic markers were measured.
Results:
SF-EVs (∼261 nm; ∼7 × 108 particles/mL) expressed canonical EV markers. In synoviocytes, SF-EVs reduced IL-1β-induced proliferation and decreased IL-6 and MMP-3 while increasing hyaluronic acid (HA). In chondrocytes, SF-EVs reduced IL-6 and MMP-13 and enhanced HA and IL-1Ra production, with sustained effects over time.
Conclusion:
These findings suggest that SF-EVs can modulate inflammatory and matrix-related responses in joint-resident cells under IL-1β-induced inflammatory conditions. Their distinct effects on synoviocytes and chondrocytes highlight the potential role of SF-EVs in regulating cell-specific responses within the osteoarthritic joint and warrant further investigation into their contribution to OA pathophysiology.
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