The Effect of Age and Intrinsic Aerobic Exercise Capacity on the Expression of Inflammation and Remodeling Markers in Rat Achilles Tendons

GND
1252288611
Zugehörigkeit
Experimental Trauma Surgery, Department of Trauma, Hand and Reconstructive Surgery, Jena University Hospital
Kinitz, Runa;
GND
1218260580
ORCID
0000-0002-1401-4679
Zugehörigkeit
Department of Cardiothoracic Surgery, Jena University Hospital
Heyne, Estelle;
ORCID
0000-0002-2019-5939
Zugehörigkeit
Department of Physiology and Pharmacology, University of Toledo, Toledo, OH 43606, USA;
Koch, Lauren G.;
Zugehörigkeit
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-5048, USA;
Britton, Steven L.;
GND
1272638774
Zugehörigkeit
Experimental Trauma Surgery, Department of Trauma, Hand and Reconstructive Surgery, Jena University Hospital
Thierbach, Manuela;
GND
120936208
ORCID
0000-0002-8365-1188
Zugehörigkeit
Experimental Trauma Surgery, Department of Trauma, Hand and Reconstructive Surgery, Jena University Hospital
Wildemann, Britt

Old age, adiposity, and metabolic disorders are known as risk factors for chronic tendinopathy, which is a common problem in both athletes and the general population. However, the importance of these influencing factors has not yet been well understood. This study investigated alterations in gene expression and histology of Achilles tendons of young (10 weeks) and old (100 weeks) rats bred for low (low capacity runners, LCR) and high (high capacity runners, HCR) intrinsic aerobic exercise capacity. In this rat model, LCR displayed a phenotype of reduced exercise capacity, higher body weight, and metabolic dysfunctions compared to HCR. We hypothesized that the risk factors for tendinopathy in old LCR could lead to more pronounced impairments in Achilles tendon tissue. In quantitative real-time PCR (qPCR), age-related downregulation of tenocyte markers e.g., tenomodulin, genes related to matrix modeling and remodeling (e.g., collagens, elastin, biglycan, fibronectin, tenascin C) as well as transforming growth factor beta 3 ( Tgfb3 ) have been detected. Inflammation marker cyclooxygenase 2 ( Cox2 ) was downregulated in old rats, while microsomal prostaglandin E synthase 2 ( Ptges2 ) was upregulated in old HCR and old LCR. In all groups, interleukin 6 ( Il6 ), interleukin 1 beta ( Il1b ), and tumor necrosis factor alpha ( Tnfa ) showed no significant alteration. In histological evaluation, tendons of old rats had fewer and more elongated tenocyte nuclei than young rats. Even though a higher content of glycosaminoglycans, a sign of degeneration, was found in old HCR and LCR, no further signs of tendinopathy were detectable in tendons of old rats by histological evaluation. Low intrinsic aerobic exercise capacity and the associated phenotype did not show significant effects on gene expression and tendon histology. These findings indicate that aging seems to play a prominent role in molecular and structural alterations of Achilles tendon tissue and suggests that other risk factors associated with intrinsic aerobic exercise capacity are less influential in this rat model.

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