Biomechanical origins of inherent tension in fibrin networks.
Biomechanical origins of inherent tension in fibrin networks.
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DOI：
10.1016/j.jmbbm.2022.105328
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发表时间：
2022-09
影响因子：
3.9
通讯作者：
Purohit, Prashant K.
中科院分区：
文献类型：
--
作者：
Spiewak, Russell;Gosselin, Andrew;Merinov, Danil;Litvinov, Rustem I.;Weisel, John W.;Tutwiler, Valerie;Purohit, Prashant K.
血凝块在血管损伤部位形成，以密封伤口并防止出血。凝块在执行其生物学功能并承受血流的流体动力学力、血管壁波动、血管外肌肉收缩和其他力时处于张力状态。有几种机制在血凝块中产生张力，其中最知名的是由活化的血小板引起的收缩/回缩。在这里，我们通过实验和建模表明，凝块张力是由纤维蛋白聚合产生的。我们的数学模型是建立在这样的假设上的，即具有双重对称性和离轴结合位点的纤维蛋白单体的形状最终是单个纤维和凝块中固有张力的来源。随着纤维直径在聚合过程中增长，纤维蛋白单体必须经受轴向扭曲变形，使得它们保持对齐以形成纤维蛋白原纤维特征的半交错排列。这种变形导致预应变，导致纤维和网络张力。我们的结果为预应变在单纤维蛋白纤维是在协议的实验中，测量它通过切割纤维和测量其松弛长度。我们使用聚合物弹性的8链模型将纤维的力学与网络的力学联系起来。通过将其与可溶胀弹性体的连续模型相结合，我们可以计算约束纤维蛋白凝胶中的张力演变。该模型预测的时间演变和拉伸应力与两个固定的流变仪板之间聚合的纤维蛋白凝块的固有张力的实验测量定性一致。这些实验还表明，增加凝血酶浓度导致纤维蛋白网络中的内部张力增加。我们的模型可以扩展到其他机制，在个别纤维产生预应变，并导致三维蛋白质聚合物网络的张力。
Blood clots form at the site of vascular injury to seal the wound and prevent bleeding. Clots are in tension as they perform their biological functions and withstand hydrodynamic forces of blood flow, vessel wall fluctuations, extravascular muscle contraction and other forces. There are several mechanisms that generate tension in a blood clot, of which the most well-known is the contraction/retraction caused by activated platelets. Here we show through experiments and modeling that clot tension is generated by the polymerization of fibrin. Our mathematical model is built on the hypothesis that the shape of fibrin monomers having two-fold symmetry and off-axis binding sites is ultimately the source of inherent tension in individual fibers and the clot. As the diameter of a fiber grows during polymerization the fibrin monomers must suffer axial twisting deformation so that they remain in register to form the half-staggered arrangement characteristic of fibrin protofibrils. This deformation results in a pre-strain that causes fiber and network tension. Our results for the pre-strain in single fibrin fibers is in agreement with experiments that measured it by cutting fibers and measuring their relaxed length. We connect the mechanics of a fiber to that of the network using the 8-chain model of polymer elasticity. By combining this with a continuum model of swellable elastomers we can compute the evolution of tension in a constrained fibrin gel. The temporal evolution and tensile stresses predicted by this model are in qualitative agreement with experimental measurements of the inherent tension of fibrin clots polymerized between two fixed rheometer plates. These experiments also revealed that increasing thrombin concentration leads to increasing internal tension in the fibrin network. Our model may be extended to account for other mechanisms that generate pre-strains in individual fibers and cause tension in three-dimensional proteinaceous polymeric networks.
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影响因子：
3.4
作者：
Li W;Sigley J;Pieters M;Helms CC;Nagaswami C;Weisel JW;Guthold M
通讯作者：
Guthold M
影响因子：
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作者：
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通讯作者：
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作者：
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作者：
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