Department of Biological Sciences, Illinois Institute of Technology, Chicago, IL.
Bioengineering Research and Development Center, Kragujevac, Serbia.
J Gen Physiol. 2021 Mar 1;153(3). doi: 10.1085/jgp.202012604.
Understanding the dynamics of a cardiac muscle twitch contraction is complex because it requires a detailed understanding of the kinetic processes of the Ca2+ transient, thin-filament activation, and the myosin-actin cross-bridge chemomechanical cycle. Each of these steps has been well defined individually, but understanding how all three of the processes operate in combination is a far more complex problem. Computational modeling has the potential to provide detailed insight into each of these processes, how the dynamics of each process affect the complexity of contractile behavior, and how perturbations such as mutations in sarcomere proteins affect the complex interactions of all of these processes. The mechanisms involved in relaxation of tension during a cardiac twitch have been particularly difficult to discern due to nonhomogeneous sarcomere lengthening during relaxation. Here we use the multiscale MUSICO platform to model rat trabecular twitches. Validation of computational models is dependent on being able to simulate different experimental datasets, but there has been a paucity of data that can provide all of the required parameters in a single experiment, such as simultaneous measurements of force, intracellular Ca2+ transients, and sarcomere length dynamics. In this study, we used data from different studies collected under similar experimental conditions to provide information for all the required parameters. Our simulations established that twitches either in an isometric sarcomere or in fixed-length, multiple-sarcomere trabeculae replicate the experimental observations if models incorporate a length-tension relationship for the nonlinear series elasticity of muscle preparations and a scheme for thick-filament regulation. The thick-filament regulation assumes an off state in which myosin heads are parked onto the thick-filament backbone and are unable to interact with actin, a state analogous to the super-relaxed state. Including these two mechanisms provided simulations that accurately predict twitch contractions over a range of different conditions.
理解心肌收缩肌搐的动力学是复杂的,因为它需要对 Ca2+ 瞬变、细肌丝激活和肌球蛋白-肌动蛋白交联的化学机械循环的动力学过程有详细的了解。这些步骤中的每一个都已经被很好地定义了,但是理解这三个过程是如何组合在一起的,是一个更为复杂的问题。计算建模有可能为这些过程中的每一个过程提供详细的见解,了解每个过程的动力学如何影响收缩行为的复杂性,以及突变等扰动如何影响所有这些过程的复杂相互作用。由于在松弛过程中肌节的非均匀伸长,舒张过程中张力松弛的机制一直特别难以辨别。在这里,我们使用多尺度 MUSICO 平台来模拟大鼠小梁肌搐。计算模型的验证取决于能够模拟不同的实验数据集,但是缺乏能够在单个实验中提供所有必需参数的数据,例如同时测量力、细胞内 Ca2+ 瞬变和肌节长度动力学。在这项研究中,我们使用了来自不同研究的数据,这些数据是在相似的实验条件下收集的,为所有必需的参数提供了信息。我们的模拟表明,如果模型包含肌肉组织非线性串联弹性的长度-张力关系和厚丝调节方案,那么在等长肌节或固定长度、多肌节小梁中的肌搐可以复制实验观察结果。厚丝调节假设一种关闭状态,其中肌球蛋白头部停留在厚丝的骨架上,无法与肌动蛋白相互作用,这种状态类似于超级松弛状态。包括这两个机制提供了模拟,能够准确地预测在一系列不同条件下的肌搐收缩。