Original article Muscle extracellular matrix degradation and contractibility following tendon rupture and disuse.
Original article Muscle extracellular matrix degradation and contractibility following tendon rupture and disuse.
复制标题
原创文章肌腱断裂和废用后的肌肉细胞外基质降解和收缩性。
DOI：
10.11138/mltj/2013.3.1.035
复制
发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Liu,Xuhui
中科院分区：
文献类型：
--
作者：
Zhang,Qia;Joshi,SunilK;Manzano,Givenchy;Lovett,DavidH;Kim,HubertT;Liu,Xuhui
肌细胞外基质（ECM）在维持肌肉完整性和力传导中起着重要作用。然而，ECM在骨骼肌萎缩中的作用尚不清楚。本研究采用两种具有临床意义的小鼠跟腱切断术和后肢悬吊模型来模拟跟腱断裂和后肢废用。治疗两周后切除腓肠肌。我们假设肌肉ECM基底膜的退化导致肌肉收缩功能障碍。我们的研究结果显示腓肠肌单次抽动力、等距强直力和肌腱断裂后收缩速度显著降低（p<0.001），但没有停止使用。此外，基质金属蛋白酶-2 （MMP-2）仅在肌腱断裂后出现上调（p=0.00234）。这些发现表明，由MMP-2引起的ECM重塑和基底膜降解可能是肌肉收缩能力下降的原因。抑制ECM降解酶可能是肌腱断裂后骨骼肌萎缩的潜在治疗策略。
Muscle extracellular matrix (ECM) plays an important role in maintaining muscular integrity and force transduction. However, the role of ECM in skeletal muscle atrophy remains unknown. In this study, we employed two clinically relevant mouse models of Achillotenotomy and hindlimb suspension to simulate Achilles tendon rupture and hindlimb disuse. The gastrocnemius was harvested following two weeks of treatment. We hypothesized that degradation of muscle ECM basement membrane lead to dysfunction of muscle contractility. Our results demonstrated a significant reduction of gastrocnemius single twitch force, isometric tetanic force, and contraction velocity following tendon rupture (p<0.001), but not disuse. Additionally, up-regulation of matrix metalloproteinase-2 (MMP-2) was observed only after tendon rupture (p=0.00234). These findings suggest that ECM remodeling and basement membrane degradation due to MMP-2 may be responsible for declined muscle contractibility. Inhibiting ECM degradation enzymes may be a potential treatment strategy for skeletal muscle atrophy after tendon rupture.