Sensing substrate rigidity by mechanosensitive ion channels with stress fibers and focal adhesions

Sensing substrate rigidity by mechanosensitive ion channels with stress fibers and focal adhesions
复制标题

DOI:
10.1016/j.ceb.2010.08.023
复制
发表时间:
2010-10-01
影响因子:
7.5
通讯作者:
Sokabe, Masahiro
Sokabe, Masahiro
中科院分区:
生物学2区
文献类型:
--
作者:
Kobayashi, Takeshi;Sokabe, Masahiro

文献摘要

被引文献

相似文献

细胞的运动、扩散、增殖和分化都受到底物刚性的严重影响。为了检测基质的刚性,细胞通过肌动蛋白应力纤维(SFS)对细胞与基质的粘连施加牵引力,并测量基质的机械响应。除了机械敏感适配子蛋白外,机械敏感(MS)通道还参与底物硬度的传感。位于灶性粘连(FAs)或其附近的MS通道通过局部改变其钙离子通透性,将SF/FA系统产生的刚性应力转化为胞浆内钙离子浓度([Ca2+]Cyt)水平。此外,在外力作用下,细胞自发产生刚性依赖的局部性[Ca~(2+)]Cyt升高,暗示MS通道是内在力测量系统。这一机制不仅可能有助于底物刚性的感知,而且可能有助于调节细胞的迁移。
Cell motility, spreading, proliferation and differentiation are critically influenced by substrate rigidity. To sense substrate rigidity, cells apply traction forces to cell-substrate adhesions via actin stress fibers (SFs) and measure mechanical responses of the substrate. Besides mechanosensitive adaptor proteins, mechanosensitive (MS) channels are involved in the substrate rigidity sensing. MS channels located at or near focal adhesions (FAs) convert the rigidity-dependent stress generated in SF/FA system into the level of cytoplasmic Ca2+ concentration ([Ca2+]cyt) by locally altering their Ca2+ permeability. Besides by external forces, cells spontaneously generate rigidity-dependent localized [Ca2+]cyt increases, implicating MS channels as intrinsic force measurement system. This mechanism may contribute to not only substrate rigidity sensing but also regulation of cell migration.