Reaction-diffusion-delay model for EPO/TNF-α interaction in articular cartilage lesion abatement.
Reaction-diffusion-delay model for EPO/TNF-α interaction in articular cartilage lesion abatement.
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DOI：
10.1186/1745-6150-7-9
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发表时间：
2012-02-21
期刊：
影响因子：
5.5
通讯作者：
Martin JA
中科院分区：
文献类型：
--
作者：
Graham JM;Ayati BP;Ding L;Ramakrishnan PS;Martin JA
关节软骨的损伤会导致软骨表面形成病变。这种病变与关节软骨变性和骨关节炎有关。典型的损伤反应通常会导致附带损伤，主要是炎症的影响，导致病变扩散到最初损伤发生的区域之外。我们提出了一个基于已知机制的最小数学模型来研究这种病变的扩散和减轻。第一种情况对应于表1中列出的参数值，而第二种情况的参数值如表2所示。特别是，我们代表了促炎和抗炎细胞因子之间的“平衡行为”，这被假设为在典型损伤反应期间软骨损伤扩张特性的主要机制。我们提出初步结果的体外研究，证实了抗炎活性的细胞因子促红细胞生成素（EPO）。我们假设细胞因子的扩散决定了损伤反应的空间行为和病变扩张，因此涉及化学物质和软骨细胞状态的反应扩散系统是表征软骨损伤反应的自然方式。我们使用数学模型给出的计算结果表明，我们的表示成功地捕获了关节软骨中损伤相关病变发展和消退的许多有趣的空间行为。此外，我们讨论了使用该模型来研究在典型损伤反应中使用EPO作为减少炎症引起的软骨附带损伤的治疗方法的可能性。图5结果的模型参数值图6结果的模型参数值本文提出的数学模型表明，抗炎细胞因子（如EPO）不仅是防止由促炎细胞因子信号传导的软骨细胞进入凋亡所必需的，而且还可能影响软骨细胞对促炎细胞因子信号传导的反应。Yang Kuang， James Faeder和Anna Marciniak-Czochra对这篇论文进行了综述。
Injuries to articular cartilage result in the development of lesions that form on the surface of the cartilage. Such lesions are associated with articular cartilage degeneration and osteoarthritis. The typical injury response often causes collateral damage, primarily an effect of inflammation, which results in the spread of lesions beyond the region where the initial injury occurs. We present a minimal mathematical model based on known mechanisms to investigate the spread and abatement of such lesions. The first case corresponds to the parameter values listed in Table 1, while the second case has parameter values as in Table 2. In particular we represent the "balancing act" between pro-inflammatory and anti-inflammatory cytokines that is hypothesized to be a principal mechanism in the expansion properties of cartilage damage during the typical injury response. We present preliminary results of in vitro studies that confirm the anti-inflammatory activities of the cytokine erythropoietin (EPO). We assume that the diffusion of cytokines determine the spatial behavior of injury response and lesion expansion so that a reaction diffusion system involving chemical species and chondrocyte cell state population densities is a natural way to represent cartilage injury response. We present computational results using the mathematical model showing that our representation is successful in capturing much of the interesting spatial behavior of injury associated lesion development and abatement in articular cartilage. Further, we discuss the use of this model to study the possibility of using EPO as a therapy for reducing the amount of inflammation induced collateral damage to cartilage during the typical injury response. Model Parameter Values for Results in Figure 5 Model Parameter Values for Results in Figure 6 The mathematical model presented herein suggests that not only are anti-inflammatory cy-tokines, such as EPO necessary to prevent chondrocytes signaled by pro-inflammatory cytokines from entering apoptosis, they may also influence how chondrocytes respond to signaling by pro-inflammatory cytokines. This paper has been reviewed by Yang Kuang, James Faeder and Anna Marciniak-Czochra.
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