Human Fetal Cartilage-Derived Progenitor Cells Exhibit AntiInflammatory Effect on IL-1β-Mediated Osteoarthritis Phenotypes In Vitro
- Affiliations
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- 1Department of Physiology and Biophysics, Inha University College of Medicine, Incheon 22212, Korea
- 2Department of Molecular Science and Technology, Ajou University, Suwon 16499, Korea
- 3Cell Therapy Center, Ajou University Medical Center, Suwon 16499, Korea
- 4Department of Biomedical Sciences, Inha University College of Medicine, 100 Inha-ro, Michuhol-gu, Incheon 22212, Korea
- 5Department of Biomedical Engineering, Pukyong National University, Pusan 48513, Korea
Abstract
- BACKGROUND
In this study, we have investigated whether human fetal cartilage progenitor cells (hFCPCs) have antiinflammatory activity and can alleviate osteoarthritis (OA) phenotypes in vitro.
METHODS
hFCPCs were stimulated with various cytokines and their combinations and expression of paracrine factors was examined to find an optimal priming factor. Human chondrocytes or SW982 synoviocytes were treated with interleukin-1β (IL-1β) to produce OA phenotype, and co-cultured with polyinosinic-polycytidylic acid (poly(I-C))-primed hFCPCs to address their anti-inflammatory effect by measuring the expression of OA-related genes. The effect of poly(I-C) on the surface marker expression and differentiation of hFCPCs into 3 mesodermal lineages was also examined.
RESULTS
Among the priming factors tested, poly(I-C) (1 μg/mL) most significantly induced the expression of paracrine factors such as indoleamine 2,3-dioxygenase, histocompatibility antigen, class I, G, tumor necrosis factor- stimulated gene-6, leukemia inhibitory factor, transforming growth factor-β1 and hepatocyte growth factor from hFCPCs. In the OA model in vitro, co-treatment of poly(I-C)-primed hFCPCs significantly alleviated IL-1b-induced expression of inflammatory factors such as IL-6, monocyte chemoattractant protein-1 and IL-1β, and matrix metalloproteinases in SW982, while it increased the expression of cartilage extracellular matrix such as aggrecan and collagen type II in human chondrocytes. We also found that treatment of poly(I-C) did not cause significant changes in the surface marker profile of hFCPCs, while showed some changes in the 3 lineages differentiation.
CONCLUSION
These results suggest that poly(I-C)-primed hFCPCs have an ability to modulate inflammatory response and OA phenotypes in vitro and encourage further studies to apply them in animal models of OA in the future.