在大鼠模型中,16周的高速跑步不足以引起跟腱病变。

IF 5 2区 生物学 Q2 CELL BIOLOGY
Snehal S Shetye, Margaret K Tamburro, Ashley K Fung, Thomas P Leahy, Madison N Magee, Harina A Raja, Stephanie N Weiss, Courtney A Nuss, Daniel C Farber, Louis J Soslowsky
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引用次数: 0

摘要

尽管跟腱病的发病率很高,但缺乏临床相关的跟腱病动物模型。先前的研究表明,高速跑步可能导致肌腱病变细胞和基质的变化,但这些变化的一致性以及功能和机械后果尚不清楚。我们试图通过定义16周高速跑步(26.8米/分钟,60分钟/天,5天/周)后跟腱结构、功能和力学的变化来确定该方案作为肌腱病变模型的适用性。我们预计高速跑步会导致有害的结构、功能和机械变化,并在16周的治疗过程中恶化。跑步机跑步确实影响体重、后肢步态和肌腱横截面积。然而,与我们的假设相反,跑步机并不会引起基质组织、细胞形态或肌腱力学的肌腱病变改变。因此,需要在临床前动物模型中稳健且可重复地诱导跟腱病变的替代策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sixteen Weeks of High-Speed Treadmill Running is Insufficient to Induce Achilles Tendinopathy in a Rat Model.

Despite the high prevalence of Achilles tendinopathy, clinically-relevant animal models of Achilles tendinopathy are lacking. Previous studies have demonstrated possible tendinopathic cell and matrix changes with high-speed treadmill running, but the consistency as well as functional and mechanical consequences of these changes were unclear. We sought to determine the applicability of this protocol as a tendinopathy model by defining changes in Achilles tendon structure, function, and mechanics associated with 16 weeks of high-speed treadmill running (26.8 m/min, 60 min/day, 5 days/week). We expected high-speed running would induce detrimental structural, functional, and mechanical changes that worsen over the course of the 16-week protocol. Treadmill running did influence bodyweight, hindlimb gait, and tendon cross-sectional area. However, contrary to our hypothesis, treadmill running did not induce tendinopathic changes in matrix organization, cell morphology, or tendon mechanics. As such, alternative strategies for robust and reproducible induction of Achilles tendinopathy in pre-clinical animal models are needed.

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来源期刊
CiteScore
9.10
自引率
1.80%
发文量
252
审稿时长
1 months
期刊介绍: The American Journal of Physiology-Cell Physiology is dedicated to innovative approaches to the study of cell and molecular physiology. Contributions that use cellular and molecular approaches to shed light on mechanisms of physiological control at higher levels of organization also appear regularly. Manuscripts dealing with the structure and function of cell membranes, contractile systems, cellular organelles, and membrane channels, transporters, and pumps are encouraged. Studies dealing with integrated regulation of cellular function, including mechanisms of signal transduction, development, gene expression, cell-to-cell interactions, and the cell physiology of pathophysiological states, are also eagerly sought. Interdisciplinary studies that apply the approaches of biochemistry, biophysics, molecular biology, morphology, and immunology to the determination of new principles in cell physiology are especially welcome.
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