Cell shape provides global control of focal adhesion assembly
Cell shape provides global control of focal adhesion assembly
复制标题
DOI：
10.1016/s0006-291x(03)01165-3
复制
发表时间：
2003-07-25
影响因子：
3.1
通讯作者：
Ingber, DE
中科院分区：
文献类型：
--
作者：
Chen, CS;Alonso, JL;Ingber, DE
通过在不同大小（100-2500μm（2））和形状（方形、圆形和线形）的单个粘附岛上或在许多较小（3-5μm直径）的圆形岛上培养细胞来控制细胞铺展，这些圆形岛涂有饱和密度的纤连蛋白并由非粘附区域分开。在所有条件下，含有纽蛋白和磷酸酪氨酸的粘着斑（FA）的数量与细胞扩散成正比。 FA 沿着经历最高张力应力的小岛的外围不对称地定位，当用凝血酶刺激细胞骨架张力时，FA 染色增加，而收缩性抑制剂促进 FA 解体。因此，这些发现证明存在一种“由内而外”的机制，通过这种机制，整体细胞变形会导致细胞骨架张力的增加，进而反馈驱动 FA 组装的局部变化。细胞形态、力学和粘附之间的这种复杂的相互作用可能对于细胞如何从活组织中整合并在其中发挥作用至关重要。 (C) 2003 Elsevier Inc. 保留所有权利。
Cell spreading was controlled independently of the amount and density of immobilized integrin ligand by culturing cells on single adhesive islands of different sizes (100-2500 mum(2)) and shapes (squares, circles, and lines) or on many smaller (3-5 mum diameter) circular islands that were coated with a saturating density of fibronectin and separated by non-adhesive regions. The amount of focal adhesions (FAs) containing vinculin and phosphotyrosine increased in direct proportion to cell spreading under all conditions. FAs localized asymmetrically along the periphery of the small islands that experienced highest tensional stress, and FA staining increased when cytoskeletal tension was stimulated with thrombin, whereas inhibitors of contractility promoted FA disassembly. Thus, these findings demonstrate the existence of an "inside-out" mechanism whereby global cell distortion produces increases in cytoskeletal tension that feed back to drive local changes in FA assembly. This complex interplay between cell morphology, mechanics, and adhesion may be critical to how cells integrate from and function in living tissues. (C) 2003 Elsevier Inc. All rights reserved.