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Computational model of wound healing: EGF secreted by fibroblasts promotes delayed re-epithelialization of epithelial keratinocytes
Integrative Biology ( IF 1.5 ) Pub Date : 2018-09-12 , DOI: 10.1039/c8ib00048d Vivi Andasari 1 , Dongyuan Lü , Maciej Swat , Shiliang Feng , Fabian Spill , Li Chen , Xiangdong Luo , Muhammad Zaman , Mian Long
Integrative Biology ( IF 1.5 ) Pub Date : 2018-09-12 , DOI: 10.1039/c8ib00048d Vivi Andasari 1 , Dongyuan Lü , Maciej Swat , Shiliang Feng , Fabian Spill , Li Chen , Xiangdong Luo , Muhammad Zaman , Mian Long
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It is widely agreed that keratinocyte migration plays a crucial role in wound re-epithelialization. Defects in this function contribute to wound reoccurrence causing significant clinical problems. Several in vitro studies have shown that the speed of migrating keratinocytes can be regulated by epidermal growth factor (EGF) which affects keratinocyte's integrin expression. The relationship between integrin expression (through cell–matrix adhesion) stimulated by EGF and keratinocyte migration speed is not linear since increased adhesion, due to increased integrin expression, has been experimentally shown to slow down cell migration due to the biphasic dependence of cell speed on adhesion. In our previous work we showed that keratinocytes that were co-cultured with EGF-enhanced fibroblasts formed an asymmetric migration pattern, where, the cumulative distances of keratinocytes migrating toward fibroblasts were smaller than those migrating away from fibroblasts. This asymmetric pattern is thought to be provoked by high EGF concentration secreted by fibroblasts. The EGF stimulates the expression of integrin receptors on the surface of keratinocytes migrating toward fibroblasts via paracrine signaling. In this paper, we present a computational model of keratinocyte migration that is controlled by EGF secreted by fibroblasts using the Cellular Potts Model (CPM). Our computational simulation results confirm the asymmetric pattern observed in experiments. These results provide a deeper insight into our understanding of the complexity of keratinocyte migration in the presence of growth factor gradients and may explain re-epithelialization failure in impaired wound healing.
中文翻译：
伤口愈合的计算模型：成纤维细胞分泌的EGF促进上皮角质形成细胞延迟再上皮化
人们普遍认为角质形成细胞迁移在伤口上皮再生中起着至关重要的作用。该功能的缺陷会导致伤口复发，从而导致严重的临床问题。多项体外研究表明，角质形成细胞迁移的速度可以通过影响角质形成细胞整合素表达的表皮生长因子（EGF）来调节。 EGF 刺激的整合素表达（通过细胞-基质粘附）与角质形成细胞迁移速度之间的关系不是线性的，因为整合素表达增加导致的粘附增加，已被实验证明由于细胞速度的双相依赖性而减慢细胞迁移。附着力。在我们之前的工作中，我们发现与EGF增强的成纤维细胞共培养的角质形成细胞形成不对称的迁移模式，其中，角质形成细胞向成纤维细胞迁移的累积距离小于远离成纤维细胞的累积距离。这种不对称模式被认为是由成纤维细胞分泌的高浓度 EGF 引起的。 EGF 刺激角质形成细胞表面整合素受体的表达，通过旁分泌信号向成纤维细胞迁移。在本文中，我们使用细胞波茨模型（CPM）提出了一种角质形成细胞迁移的计算模型，该模型由成纤维细胞分泌的 EGF 控制。我们的计算模拟结果证实了实验中观察到的不对称模式。这些结果使我们更深入地了解生长因子梯度存在下角质形成细胞迁移的复杂性，并可能解释受损伤口愈合中的上皮再形成失败。
更新日期：2018-09-12
中文翻译：
伤口愈合的计算模型：成纤维细胞分泌的EGF促进上皮角质形成细胞延迟再上皮化
人们普遍认为角质形成细胞迁移在伤口上皮再生中起着至关重要的作用。该功能的缺陷会导致伤口复发，从而导致严重的临床问题。多项体外研究表明，角质形成细胞迁移的速度可以通过影响角质形成细胞整合素表达的表皮生长因子（EGF）来调节。 EGF 刺激的整合素表达（通过细胞-基质粘附）与角质形成细胞迁移速度之间的关系不是线性的，因为整合素表达增加导致的粘附增加，已被实验证明由于细胞速度的双相依赖性而减慢细胞迁移。附着力。在我们之前的工作中，我们发现与EGF增强的成纤维细胞共培养的角质形成细胞形成不对称的迁移模式，其中，角质形成细胞向成纤维细胞迁移的累积距离小于远离成纤维细胞的累积距离。这种不对称模式被认为是由成纤维细胞分泌的高浓度 EGF 引起的。 EGF 刺激角质形成细胞表面整合素受体的表达，通过旁分泌信号向成纤维细胞迁移。在本文中，我们使用细胞波茨模型（CPM）提出了一种角质形成细胞迁移的计算模型，该模型由成纤维细胞分泌的 EGF 控制。我们的计算模拟结果证实了实验中观察到的不对称模式。这些结果使我们更深入地了解生长因子梯度存在下角质形成细胞迁移的复杂性，并可能解释受损伤口愈合中的上皮再形成失败。
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