Temporal effect of in vivo tendon fatigue loading on the apoptotic response explained in the context of number of fatigue loading cycles and initial damage parameters.

Temporal effect of in vivo tendon fatigue loading on the apoptotic response explained in the context of number of fatigue loading cycles and initial damage parameters.
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DOI:
10.1002/jor.22639
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发表时间:
2014-09
影响因子:
2.8
通讯作者:
Flatow, Evan L.
Flatow, Evan L.
中科院分区:
医学3区
文献类型:
--
作者:
Andarawis-Puri, Nelly;Philip, Anaya;Laudier, Damien;Schaffler, Mitchell B.;Flatow, Evan L.

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损伤的累积是肌腱病发展的主要因素。细胞凋亡与肌腱病变有关,但对这些损伤的发生和发展的生物学机制知之甚少。我们评估了疲劳负荷后3天和7天初始诱导损伤与凋亡活性之间的关系。我们假设,更大的凋亡活性(i)将与更大的诱导损伤和更高的疲劳载荷循环次数相关,(ii)在载荷后7天将高于3天。对左侧髌腱施加疲劳载荷,进行100或7,200次循环。在疲劳加载之前和之后进行诊断测试,以确定疲劳加载对滞后、伸长率以及加载和卸载刚度(损伤参数)的影响。采用半胱天冬酶-3染色法检测髌腱细胞凋亡率。虽然在100和7,200个周期组之间发生的凋亡活性没有差异,但更大的凋亡活性与更大的诱导损伤相关。加载后7天的凋亡活性高于3天。我们预计,能够修复肌腱中诱导损伤的健康细胞数量的减少使其易于进一步损伤。
Accumulation of damage is a leading factor in the development of tendinopathy. Apoptosis has been implicated in tendinopathy, but the biological mechanisms responsible for initiation and progression of these injuries are poorly understood. We assessed the relationship between initial induced damage and apoptotic activity 3 and 7 days after fatigue loading. We hypothesized that greater apoptotic activity (i) will be associated with greater induced damage and higher number of fatigue loading cycles, and (ii) will be higher at 7 than at 3 days after loading. Left patellar tendons were fatigue loaded for either 100 or 7,200 cycles. Diagnostic tests were applied before and after fatigue loading to determine the effect of fatigue loading on hysteresis, elongation, and loading and unloading stiffness (damage parameters). Cleaved Caspase-3 staining was used to identify and calculate the percent apoptosis in the patellar tendon. While no difference in apoptotic activity occurred between the 100 and 7,200 cycle groups, greater apoptotic activity was associated with greater induced damage. Apoptotic activity was higher at 7 than 3 days after loading. We expect that the decreasing number of healthy cells that can repair the induced damage in the tendon predispose it to further injury.
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