title: Electromagnetic fields counteract IL-1β activity during chondrogenesis of bovine mesenchymal stem cells.
abstract: 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.
authors.affiliation: Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Italy. ngrlss@unife.it.
authors.forename: Alessia
authors.initials: A
authors.lastname: Ongaro
authors.affiliation: Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Italy.
authors.forename: Agnese
authors.initials: A
authors.lastname: Pellati
authors.affiliation: Laboratory of Clinical Biophysics, IGEA S.p.A, Carpi, Italy.
authors.forename: Stefania
authors.initials: S
authors.lastname: Setti
authors.affiliation: University Campus Suffolk, Waterfront Building, Neptune Quay, Ipswich, UK.
authors.forename: Federica Francesca
authors.initials: FF
authors.lastname: Masieri
authors.affiliation: Department of Cardiology, University of Ferrara, Italy.
authors.forename: Giorgio
authors.initials: G
authors.lastname: Aquila
authors.affiliation: Laboratory of Preclinical and Surgical Studies, Research Institute Codivilla Putti, Rizzoli Orthopaedic Institute, Bologna, Italy.
authors.forename: Milena
authors.initials: M
authors.lastname: Fini
authors.affiliation: Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Italy.
authors.forename: Angelo
authors.initials: A
authors.lastname: Caruso
authors.affiliation: Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Italy.
authors.forename: Monica
authors.initials: M
authors.lastname: De Mattei
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000096:biosynthesis; D002417:Cattle; D002454:Cell Differentiation; D002478:Cells, Cultured; D020219:Chondrogenesis; D004574:Electromagnetic Fields; D005260:Female; D053583:Interleukin-1beta / Q000494:pharmacology*; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000378:metabolism*; D053782:Transforming Growth Factor beta3 / Q000494:pharmacology*
chemical_list: D000943:Antigens, Differentiation; D053583:Interleukin-1beta; D053782:Transforming Growth Factor beta3