Gluteal adipose-derived stem cell exosomes promote macrophage polarization and cartilage regeneration in osteoarthritis via PTPRC modulation.
Chen KT., Huang CC., Yadav VK., Pikatan NW., Fong IH., Kuo KT.
Animal Study on Osteoarthritis, Cartilage Damage, Meniscus Injury, Chronic Inflammation, published in Biomed Pharmacother (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Animal Study
- Journal
- Biomed Pharmacother (2026)
- Country
- France
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41740370
- DOI
- 10.1016/j.biopha.2026.119130
Abstract (original English)
Osteoarthritis (OA) is a progressive joint disease characterized by cartilage degradation, synovial inflammation, and limited regenerative capacity. Adipose-derived stem cell exosomes (ADSC-Exo) represent a promising cell-free therapeutic approach due to their immunomodulatory properties. Gluteal ADSC-Exo were isolated and characterized by nanoparticle tracking analysis and Western blotting. Their effects were evaluated in vitro in human chondrocytes, fibroblast-like synoviocytes, and THP-1-derived macrophages using proliferation, migration, immunofluorescence, Seahorse metabolic analysis, and RNA sequencing. In vivo, OA was induced in mice by destabilization of the medial meniscus (DMM) and treated with ADSC-Exo, a protein tyrosine phosphatase receptor type C (PTPRC/CD45) inhibitor alone, or in combination. Cartilage pathology and inflammation were assessed by histology, Osteoarthritis Research Society International (OARSI) scoring, immunohistochemistry, and enzyme-linked immunosorbent assays. CRISPR/Cas9-mediated deletion of PTPRC was performed in M1-polarized macrophages to validate mechanistic involvement. ADSC-Exo enhanced cell proliferation, migration, and extracellular matrix gene expression while suppressing catabolic markers under inflammatory conditions. ADSC-Exo promoted macrophage polarization toward an anti-inflammatory M2 phenotype, reduced pro-inflammatory cytoki
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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