Lavagnino Michael, Arnoczky Steven P, Kepich Eugene, Caballero Oscar, Haut Roger C
Laboratory for Comparative Orthopaedic Research, College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824, USA.
Biomech Model Mechanobiol. 2008 Oct;7(5):405-16. doi: 10.1007/s10237-007-0104-z. Epub 2007 Sep 28.
The importance of fluid-flow-induced shear stress and matrix-induced cell deformation in transmitting the global tendon load into a cellular mechanotransduction response is yet to be determined. A multiscale computational tendon model composed of both matrix and fluid phases was created to examine how global tendon loading may affect fluid-flow-induced shear stresses and membrane strains at the cellular level. The model was then used to develop a quantitative experiment to help understand the roles of membrane strains and fluid-induced shear stresses on the biological response of individual cells. The model was able to predict the global response of tendon to applied strain (stress, fluid exudation), as well as the associated cellular response of increased fluid-flow-induced shear stress with strain rate and matrix-induced cell deformation with strain amplitude. The model analysis, combined with the experimental results, demonstrated that both strain rate and strain amplitude are able to independently alter rat interstitial collagenase gene expression through increases in fluid-flow-induced shear stress and matrix-induced cell deformation, respectively.
在将整体肌腱负荷转化为细胞机械转导反应过程中，流体流动诱导的剪切应力和基质诱导的细胞变形的重要性尚未确定。创建了一个由基质和流体相组成的多尺度计算肌腱模型，以研究整体肌腱负荷如何在细胞水平上影响流体流动诱导的剪切应力和膜应变。然后使用该模型开展定量实验，以帮助理解膜应变和流体诱导的剪切应力对单个细胞生物学反应的作用。该模型能够预测肌腱对施加应变（应力、液体渗出）的整体反应，以及流体流动诱导的剪切应力随应变率增加和基质诱导的细胞变形随应变幅度增加的相关细胞反应。模型分析与实验结果相结合表明，应变率和应变幅度分别通过增加流体流动诱导的剪切应力和基质诱导的细胞变形，能够独立改变大鼠间质胶原酶基因表达。
