Roy P, Petroll W M, Cavanagh H D, Jester J V
Department of Biomedical Engineering, University of Texas Southwestern Medical Center, Dallas 75235-9057, USA.
Cell Motil Cytoskeleton. 1999;43(1):23-34. doi: 10.1002/(SICI)1097-0169(1999)43:1<23::AID-CM3>3.0.CO;2-M.
Although it is understood that cells exert mechanical forces on the extracellular matrix to promote structural organization, the exact mechanism of force transduction is not clearly understood. Using an in vitro force measurement assay, we evaluated two opposing conditions that inhibit or promote matrix organization by fibroblasts: serum deprivation and lysophosphatidic acid stimulation. Under serum deprivation, in spite of significant cell spreading and pseudopodial motility, rabbit corneal fibroblasts generated little or no force on the matrix within 2 h of observation. Lysophosphatidic acid stimulation of serum-starved cells caused dramatic cell contraction (within 2 min), which correlated temporally with a rapid increase in the tractional force generation on the matrix (0.52 x 10(-7) - 1.9 x 10(-7) N; n = 7 experiments). No cell translocation was observed during the period of force generation in response to lysophosphatidic acid-stimulation. These findings, taken together with a concomitant up-regulation of stress fibers in lysophosphatidic acid stimulated fibroblasts, indicate that contractility of non-motile cells involved in forming stress fibers and strong cell-matrix adhesion is the principal force-generating mechanism involved in matrix organization.
虽然人们知道细胞会对细胞外基质施加机械力以促进结构组织化，但力转导的确切机制尚不清楚。我们使用体外力测量分析方法，评估了两种由成纤维细胞抑制或促进基质组织化的相反条件：血清剥夺和溶血磷脂酸刺激。在血清剥夺条件下，尽管兔角膜成纤维细胞有显著的细胞铺展和伪足运动，但在观察的2小时内对基质产生的力很小或没有。用溶血磷脂酸刺激血清饥饿的细胞会导致细胞急剧收缩（在2分钟内），这在时间上与基质上牵引力产生的快速增加相关（0.52×10⁻⁷ - 1.9×10⁻⁷牛；n = 7次实验）。在对溶血磷脂酸刺激产生力的期间未观察到细胞移位。这些发现与溶血磷脂酸刺激的成纤维细胞中应激纤维的伴随上调一起，表明参与形成应激纤维和强细胞 - 基质粘附的非运动细胞的收缩性是基质组织化中涉及的主要力产生机制。
