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Effects of regenerative radioelectric asymmetric conveyer treatment on human normal and osteoarthritic chondrocytes exposed to IL-1β. A biochemical and morphological study

Authors Collodel G, Fioravanti A, Pascarelli NA, Lamboglia A, Fontani V, Maioli M, Santaniello S, Pigliaru G, Castagna A, Moretti E, Iacoponi F, Rinaldi S, Ventura C

Received 2 January 2013

Accepted for publication 31 January 2013

Published 19 March 2013 Volume 2013:8 Pages 309—316

DOI https://doi.org/10.2147/CIA.S42229

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2


Giulia Collodel,1 Antonella Fioravanti,2 Nicola Antonio Pascarelli,2 Antonello Lamboglia,2 Vania Fontani,3 Margherita Maioli,3–5 Sara Santaniello,4,5 Gianfranco Pigliaru,4,5 Alessandro Castagna,3 Elena Moretti,1 Francesca Iacoponi,1 Salvatore Rinaldi,3 Carlo Ventura3,5,6

1Department of Biomedical Sciences (Applied Biology), 2Department of Clinical Medicine and Immunological Sciences (Rheumatology Unit), University of Siena, Siena, Italy; 3Department of Regenerative Medicine, Rinaldi Fontani Institute, Florence, Italy; 4Department of Biomedical Sciences, University of Sassari, Sassari, Italy; 5Laboratory of Molecular Biology and Stem Cell Engineering, National Institute of Biostructures and Biosystems, Bologna, Italy; 6Cardiovascular Department, S Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy

Purpose: Osteoarthritis (OA) is a degenerative disease characterized by a progressive loss of articular cartilage extracellular matrix and is due to functional impairments occurring in chondrocytes. In previous works, we highlighted that Regenerative Tissue Optimization (TO-RGN) treatment with radioelectric asymmetric conveyer (REAC) technology influenced the gene expression profiles controlling stem cell differentiation and the pluripotency of human skin-derived fibroblasts in vitro. Since interleukin-1 beta signaling has been implicated in the induction and progression of this disease (through metalloproteinase-3 synthesis and nitric oxide production), we investigated whether REAC TO-RGN might influence the biochemical and morphological changes induced by interleukin-1 beta in normal and OA chondrocytes.
Methods: The induction of metalloproteinase-3 and proteoglycan synthesis was evaluated by a solid-phase enzyme-amplified sensitivity immunoassay, and nitric oxide production was evaluated with the Griess method. Ultrastructural features were observed by transmission electron microscopy.
Results: REAC TO-RGN treatment decreased nitric oxide and metalloproteinase-3 production in normal and OA chondrocytes, while inducing an increase in proteoglycan synthesis. OA chondrocytes were more affected by REAC TO-RGN treatment than were normal chondrocytes. Ultrastructural changes confirmed that REAC TO-RGN may counteract the negative effects of interleukin-1 beta incubation.
Conclusion: The results of this in vitro study suggest that REAC TO-RGN treatment may represent a new, promising approach for the management of OA.

Keywords: human chondrocytes ultrastructure, metalloproteinase, nitric oxide, proteoglycans, REAC TO-RGN treatment

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