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细胞外流体粘度调节人类细胞间干细胞的血统和功能

Alice Amitrano^1,2, Qinling Yuan^1,2, Bhawana Agarwal^1,2

¹Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21218, USA.

Science advances

|January 1, 2025

概括

细胞外流体的粘度显著影响人类介质干细胞 (hMSC) 的分化. 高粘度促进骨质分化和免疫抑制的M2巨细胞表型,作为一个关键的物理提示.

科学领域:

生物材料科学生物材料科学
细胞生物学细胞生物学
机械生物学机械生物学

背景情况:

人类介质干细胞 (hMSCs) 已知会对基质的机械性质,如刚性和粘性弹性作出反应.
细胞外流体粘度对hMSC行为的影响,特别是与基质特性结合,仍然在很大程度上未被探索.

研究的目的:

研究细胞外流体粘度作为影响hMSC功能的物理线索的作用.
为了确定液体粘度如何影响hMSC差异化和表型,在基板上具有不同的刚性和粘性弹性.

主要方法:

利用不同的基质刚度和粘弹性与受控的细胞外流体粘度.
分析了hMSC分化途径,包括actin重塑,膜张力,离子通道活性和关键蛋白质转位.
在不同的粘度条件下对hMSC行为做出反应,评估了巨细胞表型极化.

主要成果:

升高的液体粘度将hMSC偏向于一种骨质原生表型,独立于基质特性.
增加的粘度诱导了Arp2/3-依赖的动蛋白重塑,增强了NHE1活性,并促进了hMSC的扩散.
液体粘度调节膜张力,激活TRPV4通道,流入,以及RhoA/ROCK/YAP通路,导致RUNX2核转位.
在软凝上高粘度培养的hMSCs有利于M2巨细胞表型.

结论:

细胞外流体粘度是一个关键的物理线索,它决定了hMSC的分化,传递了骨质性记忆.
高粘度促进骨质生成,并诱导免疫抑制的M2巨体表型,突出其在再生医学和组织工程中的潜力.

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