Mechanical analysis of single myocyte contraction in a 3-D elastic matrix.
Mechanical analysis of single myocyte contraction in a 3-D elastic matrix.
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DOI：
10.1371/journal.pone.0075492
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Chen-Izu Y
中科院分区：
文献类型：
--
作者：
Shaw J;Izu L;Chen-Izu Y
心肌细胞在每次心跳期间经历机械应力。病理条件下过度的机械应力导致心脏功能和结构重塑，导致心脏疾病，但其确切机制仍不完全清楚。为了研究细胞和分子水平的力学转导机制，我们开发了一种新的“细胞凝胶”实验系统，在主动收缩过程中对单个心肌细胞施加多轴（3-D）应力。将分离的肌细胞包埋在弹性水凝胶中以模拟心肌中的机械环境（后负荷）。当电刺激时，凝胶内肌细胞收缩，而基质抵抗细胞的缩短和加宽，对细胞施加正常应力和剪切应力。在这里，我们提供了一个力学分析，Eshelby夹杂物问题的基础上，在弹性矩阵收缩过程中的3-D应变和应力的内部和外部的单个肌细胞。(1)肌细胞的缩短率取决于细胞的几何尺寸和细胞与凝胶的相对刚度。细长或较软的细胞缩短率较小。一个典型尺寸的肌细胞嵌入类似弹性刚度的凝胶中，只能收缩其无负荷值的20%。(2)电池内部的纵向应力约为横向应力水平的15倍。(3)细胞表面的牵引力高度不均匀，在其末端附近达到最大值，在闰盘位置显示出“热点”。(4)心肌细胞的机械能消耗随着基质刚度的增加呈单调非线性增加。我们的力学分析提供了分析解决方案，很容易借给自己的参数研究。由此产生的应变和应力状态的3-D映射用于分析和解释正在进行的细胞凝胶实验，数学模型提供了一个重要的工具来破译和量化心肌细胞中的机械转导机制。
Cardiac myocytes experience mechanical stress during each heartbeat. Excessive mechanical stresses under pathological conditions cause functional and structural remodeling that lead to heart diseases, yet the precise mechanisms are still incompletely understood. To study the cellular and molecular level mechanotransduction mechanisms, we developed a new ‘cell-in-gel’ experimental system to exert multiaxial (3-D) stresses on a single myocyte during active contraction. Isolated myocytes are embedded in an elastic hydrogel to simulate the mechanical environment in myocardium (afterload). When electrically stimulated, the in-gel myocyte contracts while the matrix resists shortening and broadening of the cell, exerting normal and shear stresses on the cell. Here we provide a mechanical analysis, based on the Eshelby inclusion problem, of the 3-D strain and stress inside and outside the single myocyte during contraction in an elastic matrix. (1) The fractional shortening of the myocyte depends on the cell’s geometric dimensions and the relative stiffness of the cell to the gel. A slender or softer cell has less fractional shortening. A myocyte of typical dimensions embedded in a gel of similar elastic stiffness can contract only 20% of its load-free value. (2) The longitudinal stress inside the cell is about 15 times the transverse stress level. (3) The traction on the cell surface is highly non-uniform, with a maximum near its ends, showing ‘hot spots’ at the location of intercalated disks. (4) The mechanical energy expenditure of the myocyte increases with the matrix stiffness in a monotonic and nonlinear manner. Our mechanical analyses provide analytic solutions that readily lend themselves to parametric studies. The resulting 3-D mapping of the strain and stress states serve to analyze and interpret ongoing cell-in-gel experiments, and the mathematical model provides an essential tool to decipher and quantify mechanotransduction mechanisms in cardiac myocytes.
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影响因子：
56.9
作者：
Prosser, Benjamin L.;Ward, Christopher W.;Lederer, W. J.
通讯作者：
Lederer, W. J.
影响因子：
10.8
作者：
EVANS, SJ;LEVI, AJ;JONES, JV
通讯作者：
JONES, JV
影响因子：
21.3
作者：
Petroff, MGV;Kim, SH;Sollott, SJ
通讯作者：
Sollott, SJ
影响因子：
7.5
作者：
Gautel, Mathias
通讯作者：
Gautel, Mathias
DOI：
10.1098/rspa.1957.0133
发表时间：
1957-01-01
影响因子：
--
作者：
ESHELBY, JD
通讯作者：
ESHELBY, JD