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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Minimal systems analysis of mitochondria-dependent apoptosis induced by cisplatin
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Minimal systems analysis of mitochondria-dependent apoptosis induced by cisplatin

机译：顺铂诱导的线粒体依赖性细胞凋亡的最小系统分析

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Recently, it was reported that the role of mitochondria-reactive oxygen species (ROS) generating pathway in cisplatin-induced apoptosis is remarkable. Since a variety of molecules are involved in the pathway, a comprehensive approach to delineate the biological interactions of the molecules is required. However, quantitative modeling of the mitochondria-ROS generating pathway based on experiment and systemic analysis using the model have not been attempted so far. Thus, we conducted experiments to measure the concentration changes of critical molecules associated with mitochondrial apoptosis in both human mesothelioma H2052 and their ρ0 cells lacking mitochondrial DNA (mtDNA). Based on the experiments, a novel mathematical model that can represent the essential dynamics of the mitochondrial apoptotic pathway induced by cisplatin was developed. The kinetic parameter values of the mathematical model were estimated from the experimental data. Then, we have investigated the dynamical properties of this model and predicted the apoptosis levels for various concentrations of cisplatin beyond the range of experiments. From parametric perturbation analysis, we further found that apoptosis will reach its saturation level beyond a certain critical cisplatin concentration.
机译：最近，据报道线粒体反应性氧（ROS）生成途径在顺铂诱导的细胞凋亡中的作用是显着的。由于该途径涉及多种分子，因此需要一种全面的方法来描述分子的生物学相互作用。然而，迄今为止尚未尝试基于实验和使用该模型的系统分析对线粒体-ROS产生途径进行定量建模。因此，我们进行了实验，以测量人间皮瘤H2052和缺少线粒体DNA（mtDNA）的ρ 0 细胞中与线粒体凋亡相关的关键分子的浓度变化。在实验的基础上，开发了一种新型数学模型，可以代表顺铂诱导的线粒体凋亡途径的基本动力学。数学模型的动力学参数值是根据实验数据估算的。然后，我们研究了该模型的动力学性质，并预测了超出实验范围的各种浓度的顺铂的凋亡水平。从参量扰动分析，我们进一步发现凋亡将达到其饱和水平，超过一定的临界顺铂浓度。

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