Experimental Trauma Surgery, Department of Trauma, Hand and Reconstructive Surgery, Jena University Hospital, Friedrich Schiller University Jena, 07747 Jena, Germany.
Department of Cardiothoracic Surgery, Jena University Hospital, 07747 Jena, Germany.
Int J Mol Sci. 2021 Dec 22;23(1):79. doi: 10.3390/ijms23010079.
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 () have been detected. Inflammation marker cyclooxygenase 2 () was downregulated in old rats, while microsomal prostaglandin E synthase 2 () was upregulated in old HCR and old LCR. In all groups, interleukin 6 (), interleukin 1 beta (), and tumor necrosis factor alpha () 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.
衰老、肥胖和代谢紊乱被认为是慢性腱病的危险因素，慢性腱病在运动员和普通人群中都是一个常见问题。然而，这些影响因素的重要性尚未得到很好的理解。本研究调查了低（低容量跑步者，LCR）和高（高容量跑步者，HCR）内在有氧运动能力的年轻（10 周）和老年（100 周）大鼠的跟腱基因表达和组织学的变化。在这种大鼠模型中，与 HCR 相比，LCR 表现出运动能力降低、体重增加和代谢功能障碍的表型。我们假设，老年 LCR 中腱病的危险因素可能导致跟腱组织更明显的损伤。在定量实时 PCR（qPCR）中，年龄相关的腱细胞标志物（如 tenomodulin）、与基质建模和重塑相关的基因（如胶原、弹性蛋白、biglycan、纤维连接蛋白、tenascin C）以及转化生长因子β 3 () 的下调已被检测到。在老年大鼠中，炎症标志物环氧化酶 2 () 下调，而在老年 HCR 和老年 LCR 中，微粒体前列腺素 E 合酶 2 () 上调。在所有组中，白细胞介素 6 (),白细胞介素 1 beta () 和肿瘤坏死因子 alpha () 没有明显改变。在组织学评估中，老年大鼠的腱细胞核比年轻大鼠更少且更长。尽管在老年 HCR 和 LCR 中发现了更多的糖胺聚糖，这是一种退化的迹象，但在老年大鼠的肌腱中通过组织学评估没有发现进一步的腱病迹象。低内在有氧运动能力和相关表型对基因表达和腱组织学没有显著影响。这些发现表明，衰老似乎在跟腱组织的分子和结构改变中起着突出的作用，并表明与内在有氧运动能力相关的其他危险因素在该大鼠模型中影响较小。
Zotero 插件
