在骨骼肌纤维化的转基因小鼠模型中，胶原蛋白交联并不决定硬度。
Collagen crosslinking does not dictate stiffness in a transgenic mouse model of skeletal muscle fibrosis.
作者信息
Chapman Mark A, Pichika Rajeswari, Lieber Richard L
机构信息
Department of Bioengineering, University of California San Diego, 9500 Gilman Drive, La Jolla, CA, 92093-0863, USA.
Department of Orthopaedic Surgery, University of California San Diego, 9500 Gilman Drive, La Jolla, CA, 92093-0863, USA.
出版信息
J Biomech. 2015 Jan 21;48(2):375-8. doi: 10.1016/j.jbiomech.2014.12.005. Epub 2014 Dec 10.
Abstract
Skeletal muscle fibrosis is characterized by increases in tissue stiffness and collagen content. However, a very weak correlation exists between collagen content and stiffness in skeletal muscle. Recently, it has been hypothesized that collagen crosslinking explains tissue stiffness in fibrotic skeletal muscle. Therefore, we addressed this hypothesis by correlating tissue stiffness with lysyl-pyridinoline, hydroxylysyl-pyridinoline, and pentosidine collagen crosslinks. Stepwise regression revealed that, separate or together, collagen crosslinks did not correlate with tissue stiffness. Our result demonstrates that increased tissue stiffness in skeletal muscle fibrosis is not simply explained by increased collagen crosslinks and/or collagen crosslink density. We suggest that collagen organization may affect tissue stiffness.
摘要
骨骼肌纤维化的特征是组织硬度和胶原蛋白含量增加。然而，骨骼肌中胶原蛋白含量与硬度之间的相关性非常弱。最近，有人提出胶原蛋白交联可以解释纤维化骨骼肌的组织硬度。因此，我们通过将组织硬度与赖氨酰吡啶啉、羟赖氨酰吡啶啉和戊糖苷胶原蛋白交联进行关联来验证这一假设。逐步回归分析表明，无论是单独还是一起，胶原蛋白交联与组织硬度均无相关性。我们的结果表明，骨骼肌纤维化中组织硬度的增加不能简单地用胶原蛋白交联增加和/或胶原蛋白交联密度增加来解释。我们认为胶原蛋白的组织方式可能会影响组织硬度。
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