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Regulatory Role of Collagen V in Establishing Mechanical Properties of Tendons and Ligaments is Tissue-Dependent

机译:胶原蛋白V在建立肌腱和韧带力学性能中的调节作用是组织依赖性的

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摘要

Patients with classic (type I) Ehlers-Danlos Syndrome (EDS), characterized by heterozygous mutations in the Col5a1 and Col5a2 genes, exhibit connective tissue hyperelasticity and recurrent joint dislocations, indicating a potential regulatory role for collagen V in joint stabilizing soft tissues. This study asked whether the contribution of collagen V to the establishment of mechanical properties is tissue-dependent. We mechanically tested four different tissues from wild type and targeted collagen V-null mice: the flexor digitorum longus tendon (FDL), Achilles tendon (ACH), the anterior cruciate ligament (ACL) and the supraspinatus tendon (SST). Area was significantly reduced in the Col5a1ΔTen/ΔTen group in the FDL, ACH, and SST. Maximum load and stiffness were reduced in the Col5a1ΔTen/ΔTen group for all tissues. However, insertion site and midsubstance modulus were reduced only for the ACL and SST. This study provides evidence that the regulatory role of collagen V in extracellular matrix assembly is tissue-dependent and that joint instability in classic EDS may be caused in part by insufficient mechanical properties of the tendons and ligaments surrounding each joint.
机译:具有Col5a1和Col5a2基因杂合突变特征的经典(I型)Ehlers-Danlos综合征(EDS)患者表现出结缔组织超弹性和复发性关节脱位,表明胶原V在关节稳定软组织中具有潜在的调节作用。这项研究询问胶原蛋白V对建立机械性能的贡献是否取决于组织。我们从野生型和靶向胶原V型无效小鼠中对四种不同的组织进行了机械测试:指趾长屈肌腱(FDL),跟腱(ACH),前十字韧带(ACL)和棘上肌腱(SST)。 FDL,ACH和SST中Col5a1 ΔTen/ΔTen组的面积显着减少。 Col5a1 ΔTen/ΔTen组的所有组织的最大负荷和刚度均降低。但是,仅对于ACL和SST,插入位置和中间物质模量降低了。这项研究提供的证据表明,胶原蛋白V在细胞外基质组装中的调节作用是组织依赖性的,并且经典EDS中的关节不稳定可能部分是由于每个关节周围的肌腱和韧带的机械性能不足所致。

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