Periostin enhances paracrine effect of adipose-derived stem cells on chondrocyte proliferation, adhesion and migration.

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

Abstract (original English)

Background Articular cartilage regeneration after injury remains a difficult clinical problem. Studies have revealed that adipose-derived stem cells (ADSCs) can promote chondrocyte regeneration. This study explored the role of Periostin, a multifunctional extracellular matrix protein, in enhancing the paracrine-mediated effects of ADSCs to promote chondrocyte regeneration. Material and methods ADSCs were isolated from murine adipose tissue and characterized. Periostin was overexpressed via a lentiviral vector in ADSCs (P-ADSCs). Chondrocytes were isolated and cocultured with P-ADSCs, followed by assessing of cell viability, apoptosis, cell migration and adhesion. In addition, periostin concentrations in the co-culture medium were measured over time by ELISA and detailed densitometric analyses of signaling proteins were performed. Results Compared with control ADSCs, P-ADSCs significantly enhanced chondrocyte proliferation, reduced apoptosis, and promoted migration and adhesion. ELISA quantification revealed that chondrocytes co-cultured with P-ADSCs showed a significant decrease in pro-inflammatory cytokines of IL-1β, IL-6, IL-18 with less than 0.6 fold-changes, and a significant increase in growth factors of TGF-β, b-FGF, PDGF with more than 4 fold-changes. Moreover, qPCR and immunoblotting demonstrated upregulation of key chondrocyte markers collagen II and Sox9, and activati

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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