Tendon overload results in alterations in cell shape and increased markers of inflammation and matrix degradation.
Abstract: Tendon injury is thought to involve both damage accumulation within the matrix and an accompanying cell response. While several studies have characterized cell and matrix response in chronically injured tendons, few have assessed the initial response of tendon to overload-induced damage. In this study, we assessed cell response to cyclic loading. Fascicle bundles from the equine superficial digital flexor tendon were exposed to cyclic loading in vitro, designed to mimic a bout of high-intensity exercise. Changes in cell morphology and protein-level alterations in markers of matrix inflammation and degradation were investigated. Loading resulted in matrix damage, which was accompanied by cells becoming rounder. The inflammatory markers cyclooxygenase-2 and interleukin-6 were increased in loaded samples, as were matrix metalloproteinase-13 and the collagen degradation marker C1,2C. These results indicate upregulation of inflammatory and degradative pathways in response to overload-induced in vitro, which may be initiated by alterations in cell strain environment because of localized matrix damage. This provides important information regarding the initiation of tendinopathy, suggesting that inflammation may play an important role in the initial cell response to tendon damage. Full understanding of the early tenocyte response to matrix damage is critical in order to develop effective treatments for tendinopathy.
© 2014 The Authors. Scandinavian Journal of Medicine & Science in Sports published by John Wiley & Sons Ltd.
Publication Date: 2014-12-30 PubMed ID: 25639911DOI: 10.1111/sms.12333Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research studied how cells in horse tendons respond to heavy loads, observing indications of inflammation and breakdown in the tendon structure. The study suggests that these responses could be key in understanding the onset of a tendon disease known as tendinopathy.
Objective and Methodology
- The research aimed at understanding how the cells within a tendon react to extreme cyclic overloads that often mimic high-intensity exercise. This understanding is critical in discovering the root causes of tendinopathy, a tendon disease.
- The researchers conducted this study by subjecting bundles of fascicle, which are from the equine superficial digital flexor tendon, to cyclic loadings in a carefully controlled laboratory environment.
Findings and Analysis
- The study discovered that extreme loading resulted in damage to the matrix that makes up the tendon. This matrix damage subsequently leads to changes in cell shapes, making them rounder than usual.
- Damage to the tendon also triggered an increase in markers indicating inflammation and matrix degradation. Cyclooxygenase-2 and interleukin-6, which are markers for inflammation, were detected in higher levels in loaded samples.
- Similarly, an increase was also observed in the matrix metalloproteinase-13, a marker that relates to tissue remodelling and collagen degradation marker C1,2C, which indicates the collagen breakdown in the tendon.
Implications and Conclusions
- The study therefore suggests that heavy loading initiates upregulation of inflammatory and degradative pathways within the tendon. Furthermore, this may be triggered by changes in cell strain resulting from localized tendon damage.
- This provides vital insights into the commencement of tendinopathy, emphasizing that inflammation might play a significant role in the early cellular response to tendon damage. The research concludes that full comprehension of the initial response of tendon cells to matrix damage is key in formulating effective treatments for tendinopathy.
Cite This Article
APA
Thorpe CT, Chaudhry S, Lei II, Varone A, Riley GP, Birch HL, Clegg PD, Screen HR.
(2014).
Tendon overload results in alterations in cell shape and increased markers of inflammation and matrix degradation.
Scand J Med Sci Sports, 25(4), e381-e391.
https://doi.org/10.1111/sms.12333 Publication
Researcher Affiliations
- Institute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.
- Institute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.
- Institute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.
- Institute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.
- School of Biological Sciences, University of East Anglia, Norwich, UK.
- Institute of Orthopaedics and Musculoskeletal Science, University College London, Stanmore, UK.
- Department of Musculoskeletal Biology, Institute of Ageing and Chronic Disease, University of Liverpool, Neston, UK.
- Institute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.
MeSH Terms
- Animals
- Biomarkers / metabolism
- Cell Shape / physiology
- Cyclooxygenase 2 / metabolism
- Extracellular Matrix / metabolism
- Horses
- In Vitro Techniques
- Inflammation / enzymology
- Inflammation / metabolism
- Interleukin-6 / metabolism
- Matrix Metalloproteinase 13 / metabolism
- Matrix Metalloproteinases / metabolism
- Stress, Mechanical
- Tendons / enzymology
- Tendons / metabolism
- Tendons / pathology
Grant Funding
- MR/K006312/1 / Medical Research Council
Citations
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