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通过决策树信号-响应建模整合“粗化”材料和“微调”小分子来控制多能基质细胞迁移。

Controlling multipotent stromal cell migration by integrating "course-graining" materials and "fine-tuning" small molecules via decision tree signal-response modeling.

机构信息

Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, United States.

出版信息

Biomaterials. 2011 Oct;32(30):7524-31. doi: 10.1016/j.biomaterials.2011.06.050. Epub 2011 Jul 22.

Abstract

Biomimetic scaffolds have been proposed as a means to facilitate tissue regeneration by multi-potent stromal cells (MSCs). Effective scaffold colonization requires a control of multiple MSC responses including survival, proliferation, differentiation, and migration. As MSC migration is relatively unstudied in this context, we present here a multi-level approach to its understanding and control, integratively tuning cell speed and directional persistence to achieve maximal mean free path (MFP) of migration. This approach employs data-driven computational modeling to ascertain small molecule drug treatments that can enhance MFP on a given materials substratum. Using poly(methyl methacrylate)-graft-poly(ethylene oxide) polymer surfaces tethered with epidermal growth factor (tEGF) and systematically adsorbed with fibronectin, vitronectin, or collagen-I to present hTERT-immortalized human MSCs with growth factor and extracellular matrix cues, we measured cell motility properties along with signaling activities of EGFR, ERK, Akt, and FAK on 19 different substrate conditions. Speed was consistent on collagen/tEGF substrates, but low associated directional persistence limited MFP. Decision tree modeling successfully predicted that ERK inhibition should enhance MFP on collagen/tEGF substrates by increasing persistence. Thus, we demonstrated a two-tiered approach to control MSC migration: materials-based "coarse-graining" complemented by small molecule "fine-tuning".

摘要

仿生支架被提议作为一种通过多能基质细胞 (MSCs) 促进组织再生的方法。有效的支架定植需要控制多种 MSC 反应,包括存活、增殖、分化和迁移。由于在这种情况下 MSC 的迁移相对未被研究,我们在这里提出了一种多层面的方法来理解和控制它,综合调整细胞速度和方向持久性,以实现最大的平均自由程 (MFP) 的迁移。该方法采用数据驱动的计算建模来确定小分子药物治疗方法,以增强给定材料衬底上的 MFP。使用聚 (甲基丙烯酸甲酯)-接枝-聚 (氧化乙烯) 聚合物表面,表面连接表皮生长因子 (tEGF),并系统地吸附纤连蛋白、层粘连蛋白或胶原蛋白-I,为 hTERT 永生化人 MSC 提供生长因子和细胞外基质线索,我们在 19 种不同的基质条件下测量了细胞迁移特性以及 EGFR、ERK、Akt 和 FAK 的信号转导活性。在胶原/tEGF 基质上速度是一致的,但低方向持久性限制了 MFP。决策树模型成功预测 ERK 抑制应该通过增加持久性来提高胶原/tEGF 基质上的 MFP。因此,我们展示了一种控制 MSC 迁移的两层方法:基于材料的“粗粒化”,辅以小分子的“微调”。

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