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首页> 外文期刊>Cell motility and the cytoskeleton >Sensitivity of alveolar macrophages to substrate mechanical and adhesive properties.
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Sensitivity of alveolar macrophages to substrate mechanical and adhesive properties.

机译：肺泡巨噬细胞对基质机械和粘合特性的敏感性。

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In order to understand the sensitivity of alveolar macrophages (AMs) to substrate properties, we have developed a new model of macrophages cultured on substrates of increasing Young's modulus: (i) a monolayer of alveolar epithelial cells representing the supple (approximately 0.1 kPa) physiological substrate, (ii) polyacrylamide gels with two concentrations of bis-acrylamide representing low and high intermediate stiffness (respectively 40 kPa and 160 kPa) and, (iii) a highly rigid surface of plastic or glass (respectively 3 MPa and 70 MPa), the two latter being or not functionalized with type I-collagen. The macrophage response was studied through their shape (characterized by 3D-reconstructions of F-actin structure) and their cytoskeletal stiffness (estimated by transient twisting of magnetic RGD-coated beads and corrected for actual bead immersion). Macrophage shape dramatically changed from rounded to flattened as substrate stiffness increased from soft ((i) and (ii)) to rigid (iii) substrates, indicating a net sensitivity of alveolar macrophages to substrate stiffness but without generating F-actin stress fibers. Macrophage stiffness was also increased by large substrate stiffness increase but this increase was not due to an increase in internal tension assessed by the negligible effect of a F-actin depolymerizing drug (cytochalasine D) on bead twisting. The mechanical sensitivity of AMs could be partly explained by an idealized numerical model describing how low cell height enhances the substrate-stiffness-dependence of the apparent (measured) AM stiffness. Altogether, these results suggest that macrophages are able to probe their physical environment but the mechanosensitive mechanism behind appears quite different from tissue cells, since it occurs at no significant cell-scale prestress, shape changes through minimal actin remodeling and finally an AMs stiffness not affected by the loss in F-actin integrity.
机译：为了了解肺泡巨噬细胞（AMs）对基质特性的敏感性，我们开发了一种新的培养在杨氏模量增加的基质上的巨噬细胞模型：（i）代表柔软的（约0.1 kPa）生理状态的单层肺泡上皮细胞（ii）具有两种浓度的双丙烯酰胺的聚丙烯酰胺凝胶，分别代表低和高的中间刚度（分别为40 kPa和160 kPa），以及（iii）塑料或玻璃的高刚性表面（分别为3 MPa和70 MPa），后者是否已被I型胶原功能化。通过巨噬细胞的形状（以F-肌动蛋白结构的3D重建为特征）和细胞骨架刚度（通过磁性RGD包覆的磁珠的瞬时扭曲进行估算，并针对实际的磁珠浸没进行校正）来研究巨噬细胞的反应。随着基质刚度从柔软的（i）和（ii）变为刚性的（iii）基质，巨噬细胞的形状从圆形急剧变平，这表明肺泡巨噬细胞对基质刚度具有净敏感性，但没有产生F-肌动蛋白应力纤维。巨噬细胞刚度也因底物刚度的大幅度增加而增加，但这种增加并非归因于F-肌动蛋白解聚药物（细胞松弛素D）对微珠扭曲作用的影响可忽略不计，内部张力的增加。 AMs的机械灵敏度可以通过理想化的数值模型来部分解释，该模型描述了低像元高度如何增强表观（测量）的AM刚度对基底刚度的依赖性。总而言之，这些结果表明巨噬细胞能够探测其物理环境，但背后的机械敏感性机制却与组织细胞完全不同，因为它没有明显的细胞尺度预应力发生，通过最小的肌动蛋白重塑来改变形状，最终使AMs刚度不受影响F-肌动蛋白完整性的丧失。

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