Aging increases stiffness of cardiac myocytes measured by atomic force microscopy nanoindentation
Aging increases stiffness of cardiac myocytes measured by atomic force microscopy nanoindentation
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DOI：
10.1152/ajpheart.00564.2003
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发表时间：
2004-08-01
影响因子：
4.8
通讯作者：
Vatner, SF
中科院分区：
文献类型：
--
作者：
Lieber, SC;Aubry, N;Vatner, SF
众所周知，衰老的心脏表现出左心室（LV）舒张功能障碍和机械性能的变化，这被认为是由于细胞外基质的改变。我们验证了心肌细胞的力学特性随年龄增长而显著变化的假设，这可能有助于左室舒张功能障碍的整体变化。我们使用原子力显微镜（AFM），它确定在纳米级分辨率的肌细胞，从年轻（4个月）和老年（30个月）雄性Fischer 344 x Brown Norway F1杂交大鼠的细胞力学性质的变化。刚度的量度，即，表观弹性模量，通过分析AFM压痕力与深度之间的关系与经典的无穷小应变理论和建模的AFM探针作为一个钝锥压头。这是第一项证明单个衰老心肌细胞表观弹性模量显著增加（P < 0.01）的研究（从35.1 +/- 0.7，n = 53，增加到42.5 +/- 1.0 KPa，n = 58），支持了一个新的概念，即衰老心脏中介导LV舒张功能障碍的机制部分存在于肌细胞水平。
It is well established that the aging heart exhibits left ventricular (LV) diastolic dysfunction and changes in mechanical properties, which are thought to be due to alterations in the extracellular matrix. We tested the hypothesis that the mechanical properties of cardiac myocytes significantly change with aging, Which could contribute to the global changes in LV diastolic dysfunction. We used atomic force microscopy (AFM), which determines cellular mechanical property changes at nanoscale resolution in myocytes, from young (4 mo) and old (30 mo) male Fischer 344 x Brown Norway F1 hybrid rats. A measure of stiffness, i.e., apparent elastic modulus, was determined by analyzing the relationship between AFM indentation force and depth with the classical infinitesimal strain theory and by modeling the AFM probe as a blunted conical indenter. This is the first study to demonstrate a significant increase (P < 0.01) in the apparent elastic modulus of single, aging cardiac myocytes (from 35.1 +/- 0.7, n = 53, to 42.5 +/- 1.0 KPa, n = 58), supporting the novel concept that the mechanism mediating LV diastolic dysfunction in aging hearts resides, in part, at the level of the myocyte.