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J Tissue Eng Regen Med. 2012 Dec 17. doi: 10.1002/term.1671. [Epub ahead of print]

Electromagnetic fields counteract IL-1β activity during chondrogenesis of bovine mesenchymal stem cells.

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  • 1Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Italy.


Osteoarthritis (OA) is a common joint disease associated with articular cartilage degeneration. To improve the therapeutic options of OA, tissue engineering based on the use of mesenchymal stem cells (MSCs) has emerged. However, the presence of inflammatory cytokines, such as interleukin-1β (IL-1β), during chondrogenesis reduces the efficacy of cartilage engineering repair procedures by preventing chondrogenic differentiation. Previous studies have shown that electromagnetic fields (EMFs) stimulate anabolic processes in OA cartilage and limit IL-1β catabolic effects. We investigated the role of EMFs during chondrogenic differentiation of MSCs, isolated from bovine synovial fluid, in the absence and presence of IL-1β. Pellets of MSCs were differentiated for 3 and 5 weeks with transforming growth factor-β3 (TGFβ3), in the absence and presence of IL-1β and exposed or unexposed to EMFs. Biochemical, quantitative real-time RT-PCR and histological results showed that EMFs alone or in the presence of TGFβ3 play a limited role in promoting chondrogenic differentiation. Notably, in the presence of IL-1β and TGFβ3 a recovery of proteoglycan (PG) synthesis, PG content and aggrecan and type II collagen mRNA expression in the EMF-exposed compared to unexposed pellets was observed. Also, histological and immunohistochemical results showed an increase in staining for alcian blue, type II collagen and aggrecan in EMF-exposed pellets. In conclusion, this study shows a significant role of EMFs in counteracting the IL-1β-induced inhibition of chondrogenesis, suggesting EMFs as a therapeutic strategy for improving the clinical outcome of cartilage engineering repair procedures, based on the use of MSCs. Copyright © 2012 John Wiley & Sons, Ltd.

Copyright © 2012 John Wiley & Sons, Ltd.

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