Biophys J:基质硬度和炎症因子对MSC成骨分化的协同作用

2019-06-13 不详 网络

间充质干细胞(MSC)在体内存在于复杂的微环境中。炎症引起的微环境中生化和生物物理信号的变化都会影响MSCs的分化行为。然而,大多数研究仅关注生化或生物物理线索,尽管基质硬度和炎症因子对MSC成骨分化的协同作用尚未被探索。在这里,我们表明在人类MSCs(hMSCs)的成骨分化中存在基质刚度依赖性调节,具有更高的基质刚度,有利于成骨分化。然而,当加入白细胞介素-1β(IL-1β)时,hMSC的成骨分

间充质干细胞(MSC)在体内存在于复杂的微环境中。炎症引起的微环境中生化和生物物理信号的变化都会影响MSCs的分化行为。然而,大多数研究仅关注生化或生物物理线索,尽管基质硬度和炎症因子对MSC成骨分化的协同作用尚未被探索。

在这里,我们表明在人类MSCs(hMSCs)的成骨分化中存在基质刚度依赖性调节,具有更高的基质刚度,有利于成骨分化。然而,当加入白细胞介素-1β(IL-1β)时,hMSC的成骨分化受到抑制,这与增加的基质硬度无关。实验观察和数学模型均证实基质硬度和IL-1β可激活ERK1/2信号传导并有助于成骨分化。由IL-1β激活的p38信号传导在抑制成骨细胞分化中具有强烈作用,因此减少了ERK1/2信号传导的重要作用。此外,模型参数的灵敏度分析表明,敏感因子(如FAK,ERK和p38)的激活/失活动力学也在基质硬度和IL-1β对hMSCs成骨分化的协同作用中起关键作用。

综上所述,该研究结果为生物化学和生物物理微环境对调节MSC分化的协同效应提供了新的见解。

原始出处:

Wan W, Cheng B, et al., Synergistic Effect of Matrix Stiffness and Inflammatory Factors on Osteogenic Differentiation of MSC. Biophys J. 2019 May 25. pii: S0006-3495(19)30421-7. doi: 10.1016/j.bpj.2019.05.019. 

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    2019-08-01 sunylz
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    2019-06-15 zhaojie88
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    2019-06-15 huanbaofeng