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首页> 外文期刊>Acta biomaterialia >Force response and actin remodeling (agglomeration) in fibroblasts due to lateral indentation.
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Force response and actin remodeling (agglomeration) in fibroblasts due to lateral indentation.

机译：由于侧凹，成纤维细胞的力反应和肌动蛋白重塑（凝聚）。

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We report the loading and unloading force response of single living adherent fibroblasts due to large lateral indentation obtained by a two-component microelectromechanical systems force sensor. Strong hysteretic force response is observed for all the tested cells. For the loading process, the force response is linear (often with small initial non-linearity) to a deformation scale comparable to the undeformed cell size, followed by plastic yielding. In situ visualization of actin fibers by tagging with green fluorescent protein indicates that during the indentation process, actin network possibly decomposes irreversibly at discrete locations where well-defined circular actin agglomerates appear all over the cell, which explains the irreversibility of the force response. Similar agglomeration is observed when the cell is compressed laterally by a micro plate. The distribution pattern of the agglomerates strongly correlates with the arrangement of the actin fibers of the pre-indented cell. The size of the agglomerates increases with time as t(alpha), initially with alpha=2-3 followed by alpha=0.5-1. The higher growth rate suggests influx of actin into the agglomerates. The slower rate suggests a diffusive spreading, but the diffusion constant is two orders of magnitude lower than that of an actin monomer through the cytoplasm. Actin agglomeration has previously been observed due to biochemical treatment, gamma-radiation, and ischemic injury, and has been identified as a precursor to cell death. We believe this is the first evidence of actin agglomeration due to mechanical indentation/compression. The study demonstrates that living cells may initiate similar functionalities in response to dissimilar mechanical and biochemical stimuli.
机译：我们报告了由于两个组件微机电系统力传感器获得的较大的横向压痕，导致单个活着的粘附成纤维细胞的加载和卸载力响应。对于所有测试的细胞，观察到强烈的滞后力响应。对于加载过程，力响应是线性的（通常具有很小的初始非线性），其变形规模可与未变形的孔尺寸相比，然后是塑性屈服。通过用绿色荧光蛋白标记来原位观察肌动蛋白纤维，表明在压痕过程中，肌动蛋白网络可能在离散位置发生不可逆分解，而清晰的圆形肌动蛋白聚集物遍布整个细胞，这说明了力响应的不可逆性。当细胞被微板横向压缩时，观察到类似的团聚。附聚物的分布模式与预压痕细胞的肌动蛋白纤维的排列紧密相关。附聚物的尺寸随着时间而随着t（α）增加，最初为α＝ 2-3，随后为α＝ 0.5-1。较高的生长速率表明肌动蛋白涌入附聚物。较低的速率表明扩散扩散，但是扩散常数比肌动蛋白单体穿过细胞质的扩散常数低两个数量级。由于生化处理，伽马射线辐射和缺血性损伤，以前已经观察到肌动蛋白的团聚，并且已经确定其是细胞死亡的前兆。我们相信这是肌动蛋白由于机械压痕/压缩而聚集的第一个证据。该研究表明，活细胞可以响应不同的机械和生化刺激而启动类似的功能。

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