Sibley School of Mechanical and Aerospace Engineering, Cornell University, Ithaca, NY, USA.
Leni and Peter W. May Department of Orthopaedics, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Sci Rep. 2018 Jun 12;8(1):8933. doi: 10.1038/s41598-018-27196-5.
Tendons are ineffective at repairing sub-rupture fatigue injuries. Accordingly, we evaluated whether an exercise protocol that we have previously found to decrease structural damage kinks in fatigue damaged tendons, leads to improvement in mechanical properties. We hypothesized that exercise that promotes repair of fatigue damage will decrease apoptosis and increase the population of myofibroblasts. Rat patellar tendons underwent in vivo fatigue loading for 500 or 7200 cycles. Animals resumed cage activity for 2-weeks, then either remained cage active or began treadmill running until sacrifice at 4- or 10-weeks post-fatigue loading. Exercise following fatigue damage increased the stiffness back towards naïve levels, decreased apoptosis and increased the population of myofibroblasts. Next, proteins associated with inhibition of apoptosis (Collagen VI) or activation of myofibroblast (pSmad 2/3, fibrillin, integrin subunits αV and α5) were evaluated. Data suggests that collagen VI may not be integral to inhibition of apoptosis in this context. Exercise increased pSmad 2/3 and fibrillin in the insertion region for the 7200-cycles group. In addition, exercise decreased integrin αV and increased integrin α5 in fatigue damaged tendons. Data suggests that a decrease in apoptosis and an increase in population of myofibroblasts may be integral to remodeling of fatigue damaged tendons.
肌腱在修复亚破裂性疲劳损伤方面效果不佳。因此，我们评估了一种我们之前发现的能减少疲劳损伤肌腱结构损伤扭结的运动方案是否能改善力学性能。我们假设促进疲劳损伤修复的运动将减少细胞凋亡并增加肌成纤维细胞的数量。大鼠髌腱在体内经历了 500 或 7200 次疲劳加载。动物恢复笼内活动 2 周，然后继续保持笼内活动或开始跑步机跑步，直到疲劳加载后 4 或 10 周处死。疲劳损伤后进行运动可使肌腱刚度恢复到接近正常水平，减少细胞凋亡并增加肌成纤维细胞数量。接下来，评估了与细胞凋亡抑制（胶原 VI）或肌成纤维细胞激活（pSmad 2/3、纤维连接蛋白、整合素亚基 αV 和 α5）相关的蛋白。数据表明，胶原 VI 在这种情况下可能不是细胞凋亡抑制的必要因素。运动增加了 7200 次循环组插入区域的 pSmad 2/3 和纤维连接蛋白。此外，运动减少了疲劳损伤肌腱中的整合素 αV 并增加了整合素 α5。数据表明，细胞凋亡减少和肌成纤维细胞数量增加可能是疲劳损伤肌腱重塑的必要因素。
