Abstract
Tendinopathy is accompanied by a cascade of inflammatory events promoting tendon degeneration. Among various cytokines, interleukin-1β plays a central role in driving catabolic processes, ultimately resulting in the activation of matrix metalloproteinases and a diminished collagen synthesis, both of which promote tendon extracellular matrix degradation. Pulsed electromagnetic field (PEMF) therapy is often used for pain management, osteoarthritis, and delayed wound healing. In vitro PEMF treatment of tendon-derived cells was shown to modulate pro-inflammatory cytokines, potentially limiting their catabolic effects. However, our understanding of the underlying cellular and molecular mechanisms remains limited. We therefore investigated the transcriptome-wide responses of Il-1β-primed rat Achilles tendon cell-derived 3D tendon-like constructs to high-energy PEMF treatment. RNASeq analysis and gene ontology assignment revealed various biological processes to be affected by PEMF, including extracellular matrix remodeling and negative regulation of apoptosis. Further, we show that members of the cytoprotective Il-6/gp130 family and the Il-1β decoy receptor Il1r2 are positively regulated upon PEMF exposure. In conclusion, our results provide fundamental mechanistic insight into the cellular and molecular mode of action of PEMF on tendon cells and can help to optimize treatment protocols for the non-invasive therapy of tendinopathies.
Highlights
Tendon overuse injuries and tendinopathies represent debilitating conditions affecting both the working population and recreational athletes, and represent one of the most frequent musculoskeletal conditions for which patients seek medical advice [1]
Recent studies convincingly demonstrate that a cascade of inflammatory events, such as lymphocyte and macrophage infiltration, matrix metalloprotease (MMP) activation, and secretion of inflammatory mediators, including various cytokines, prostaglandins, and nitric oxide [5,6,7] are central to the etiology of tendinopathies
As gene ontology (GO) assignment indicated that genes involved in extracellular matrix (ECM) remodeling and collagen fibrillogenesis were affected, we examined if Pulsed electromagnetic field (PEMF) exposure results in a structural change of the 3D tendon-like constructs
Summary
Tendon overuse injuries and tendinopathies represent debilitating conditions affecting both the working population and recreational athletes, and represent one of the most frequent musculoskeletal conditions for which patients seek medical advice [1]. Cells 2019, 8, 399 tendon injuries and chronic tendinopathies remain clinically challenging [2]. Development of effective treatment strategies is currently hampered by our poor understanding of the molecular and cellular events underlying tendinopathy. In the past tendinopathy has primarily been considered as a non-inflammatory, degenerative process. Recent studies convincingly demonstrate that a cascade of inflammatory events, such as lymphocyte and macrophage infiltration, matrix metalloprotease (MMP) activation, and secretion of inflammatory mediators, including various cytokines, prostaglandins, and nitric oxide [5,6,7] are central to the etiology of tendinopathies. The key cytokines in tendon disease have not yet been fully defined, family members of the interleukin-1
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