Mechanical and biochemical modeling of cortical oscillations in spreading cells
Mechanical and biochemical modeling of cortical oscillations in spreading cells
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DOI：
10.1529/biophysj.107.121335
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发表时间：
2008-06-15
影响因子：
3.4
通讯作者：
Elston, Timothy C.
中科院分区：
文献类型：
--
作者：
Kapustina, Maryna;Weinreb, Gabriel E.;Elston, Timothy C.
基于肌动蛋白的皮质收缩性是真核细胞的共同特征，并且涉及细胞运动、细胞分裂和细胞凋亡。在非肌肉细胞中，收缩性的振荡是由细胞伸展过程中的微管解聚引起的。我们开发了一个常微分方程模型来描述这种行为。计算模型包括36个参数。除了两个模型参数外，所有参数的值都取自文献中的实验测量值。使用这些值，我们表明，该模型产生的振荡行为与目前的实验观察一致。节律性行为的发生是由于钙诱导的收缩性和牵张激活的钙通道的拮抗作用。该模型提出了几个实验可验证的预测：1）缓冲细胞内钙增加皮层振荡的周期和降低振幅; 2）增加牵张激活通道的数量或活性导致皮层振荡的周期和振幅增加; 3）抑制Ca ~（2+）泵活性增加振荡的周期和振幅;和4），对于钙浓度存在阈值，低于该阈值振荡停止。
Actomyosin-based cortical contractility is a common feature of eukaryotic cells and is involved in cell motility, cell division, and apoptosis. In nonmuscle cells, oscillations in contractility are induced by microtubule depolymerization during cell spreading. We developed an ordinary differential equation model to describe this behavior. The computational model includes 36 parameters. The values for all but two of the model parameters were taken from experimental measurements found in the literature. Using these values, we demonstrate that the model generates oscillatory behavior consistent with current experimental observations. The rhythmic behavior occurs because of the antagonistic effects of calcium-induced contractility and stretch-activated calcium channels. The model makes several experimentally testable predictions: 1), buffering intracellular calcium increases the period and decreases the amplitude of cortical oscillations; 2), increasing the number or activity of stretch activated channels leads to an increase in period and amplitude of cortical oscillations; 3), inhibiting Ca2+ pump activity increases the period and amplitude of oscillations; and 4), a threshold exists for the calcium concentration below which oscillations cease.