Homeostatic maintenance via degradation and repair of elastic fibers under tension
Homeostatic maintenance via degradation and repair of elastic fibers under tension
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DOI：
10.1038/srep27474
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发表时间：
2016-06-09
影响因子：
4.6
通讯作者：
Suki, Bela
中科院分区：
文献类型：
--
作者：
Alves, Calebe;Araujo, Ascanio D.;Suki, Bela
细胞外基质的维持需要一种有效的调节，平衡酶降解与胶原原纤维和纤维的修复。在这里，我们研究了弹性纤维在张力下的长期维持，以及与消化和修复过程相关的一般降解和再生颗粒的扩散。计算结果表明，假设细胞周期性地探测纤维刚度，以调节降解和再生颗粒的产生和释放，可以实现自稳态纤维刚度。然而，这种机制不能维持均匀的纤维。为了解释轴向均匀性，我们引入了一种强大的控制机制，该机制由施加在纤维末端的机械力如何调节粒子的结合亲和力来局部控制。该模型预测沿纤维的直径变化，与正常大鼠胸主动脉扫描电镜图像中胶原纤维直径的轴向分布一致。只有当施加在纤维上的力在沿纤维的局部刚度方差取最小值的范围内时，模型预测才与实验相符。因此，我们的模型预测，纤维的生物物理特性在这些纤维的长期调节维持中起着重要作用。
Cellular maintenance of the extracellular matrix requires an effective regulation that balances enzymatic degradation with the repair of collagen fibrils and fibers. Here, we investigate the long-term maintenance of elastic fibers under tension combined with diffusion of general degradative and regenerative particles associated with digestion and repair processes. Computational results show that homeostatic fiber stiffness can be achieved by assuming that cells periodically probe fiber stiffness to adjust the production and release of degradative and regenerative particles. However, this mechanism is unable to maintain a homogeneous fiber. To account for axial homogeneity, we introduce a robust control mechanism that is locally governed by how the binding affinity of particles is modulated by mechanical forces applied to the ends of the fiber. This model predicts diameter variations along the fiber that are in agreement with the axial distribution of collagen fibril diameters obtained from scanning electron microscopic images of normal rat thoracic aorta. The model predictions match the experiments only when the applied force on the fiber is in the range where the variance of local stiffness along the fiber takes a minimum value. Our model thus predicts that the biophysical properties of the fibers play an important role in the long-term regulatory maintenance of these fibers.