Biomechanics Laboratory, Mayo Clinic, 200 First St., Rochester, MN 55905, USA.
J Appl Physiol (1985). 2010 Dec;109(6):1762-8. doi: 10.1152/japplphysiol.00051.2010. Epub 2010 Oct 14.
Tendon disuse, or stress deprivation, frequently accompanies clinical disorders and treatments, yet the metabolism of tendons subject to stress deprivation has rarely been investigated systematically. The effects of stress deprivation on canine flexor tendon were investigated in this study. One adult canine forepaw was suspended for 21 or 42 days. Control forepaws were collected from dogs that had no intervention on their limbs and paws. The expression of collagen I and III was not significantly altered in the tendons disused for 21 days but was significantly decreased at 42 days (P < 0.03). The expression of collagen II, aggrecan, decorin, and fibronectin was significantly decreased in the tendons in the suspended limbs at 21 days (P < 0.002) and further reduced at 42 days. With stress deprivation, the expression of matrix metalloproteinase 2 (MMP2) was significantly increased (P < 0.004) at 21 and 42 days. The expression of MMP3 was significantly decreased at 21 and 42 days (P < 0.03). The expression of MMP13 was not altered with stress deprivation at 21 and 42 days. The expression of MMP14 was significantly increased at 21 days (P = 0.0015) and returned to the control level at 42 days. Tissue inhibitor of metalloproteinase 1 (TIMP1) expression was decreased after the limbs were suspended for 42 days (P = 0.0043), but not 21 days. However, TIMP2 expression was not significantly different from control at 21 or 42 days. Furthermore, the cross-sectional area of the stress-deprived tendons at 42 days was decreased compared with the control group (P < 0.01). The intervention method in this study did not result in any alteration of stiffness of the tendon. Our study demonstrated that stress deprivation decreases the anabolic process and increases the catabolic process of extracellular matrix in flexor tendon.
肌腱废用,即应力剥夺,常伴随临床疾病和治疗出现,但肌腱在受到应力剥夺后的代谢情况很少被系统地研究。本研究旨在探讨应力剥夺对犬屈肌腱的影响。一只成年犬的前肢被悬吊 21 或 42 天。对照组取自未对四肢和爪子进行干预的犬。在被悬吊 21 天的肌腱中,胶原 I 和 III 的表达没有显著改变,但在 42 天时显著降低(P < 0.03)。在被悬吊的肢体中,胶原 II、聚集蛋白聚糖、核心蛋白聚糖和纤维连接蛋白的表达在 21 天(P < 0.002)时显著降低,在 42 天时进一步降低。随着应力剥夺,基质金属蛋白酶 2(MMP2)的表达在 21 和 42 天时显著增加(P < 0.004)。MMP3 的表达在 21 和 42 天时显著降低(P < 0.03)。MMP13 的表达在 21 和 42 天内不受应力剥夺的影响。MMP14 的表达在 21 天时显著增加(P = 0.0015),42 天时恢复到对照水平。四肢悬吊 42 天后,组织金属蛋白酶抑制剂 1(TIMP1)的表达减少(P = 0.0043),但 21 天无明显差异。然而,TIMP2 的表达在 21 天和 42 天都与对照组无显著差异。此外,与对照组相比,42 天时受应力剥夺的肌腱横截面积减小(P < 0.01)。本研究中的干预方法并未导致肌腱刚度发生任何改变。我们的研究表明,应力剥夺会降低屈肌腱细胞外基质的合成代谢过程,增加其分解代谢过程。