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Updated: Sep 20, 2025
Isolation and Enrichment of Human Adipose-derived Stromal Cells for Enhanced Osteogenesis
Published on: January 12, 2015
Periostin enhances paracrine effect of adipose-derived stem cells on chondrocyte proliferation, adhesion and
Ran Lu1, Yong Hou1, Xiaogao Wang1
1Department of Vascular Surgery, the First Affiliated Hospital of Bengbu Medical University, 287 Changhuai Road, Bengbu, Anhui 233004, China.
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 activation of FAK/PI3K/Akt/ERK signals.
Conclusions:
Periostin overexpression in ADSCs enhances their paracrine effect, promoting chondrocyte proliferation, adhesion, migration, and favorable phenotypic marker expression while modulating cytokine secretion. These findings provide a potential strategy for enhancing ADSC-mediated cartilage repair.
