Tsai M A, Frank R S, Waugh R E
Department of Biophysics, University of Rochester School of Medicine and Dentistry, New York 14642.
Biophys J. 1994 Jun;66(6):2166-72. doi: 10.1016/S0006-3495(94)81012-4.
Actin is a ubiquitous protein in eukaryotic cells. It plays a major role in cell motility and in the maintenance and control of cell shape. In this article, we intend to address the contribution of actin to the passive mechanical properties of human neutrophils. As a framework for assessing this contribution, the neutrophil is modeled as a simple viscous fluid drop with a constant cortical ("surface") tension. The reagent cytochalasin B (CTB) was used to disrupt the F-actin structure, and the neutrophil cortical tension and cytoplasmic viscosity were evaluated by single-cell micropipette aspiration. The cortical tension was calculated by simple force balance, and the viscosity was calculated according to a numerical analysis of the cell entry into the micropipette. CTB reduced the cell cortical tension in a dose-dependent fashion: by 19% at a concentration of 3 microM and by 49% at 30 microM. CTB also reduced the cytoplasmic viscosity by approximately -25% at a concentration of 3 microM and by approximately 65% at a concentration of 30 microM when compared at the same aspiration pressures. All three groups of neutrophils, normal cells, and cells treated with either 3 or 30 microM CTB, exhibited non-Newtonian behavior, in that the apparent viscosity decreased with increasing shear rate. The dependence of the cytoplasmic viscosity on deformation rate can be described empirically by mu = mu c(gamma m/gamma c)-b, where mu is cytoplasmic viscosity, gamma m is mean shear rate, mu c is the characteristic viscosity at the characteristic shear rate gamma c, and b is a material coefficient. The shear rate dependence of the cytoplasmic viscosity was reduced by CTB treatment. This is reflected by the changes in the material coefficients. When gamma c was set to 1 s-1, pc = 130 +/- 23 Pa.s and b = 0.52 +/- 0.09 for normal neutrophils and pc = 54 +/- 15 Pa.S and b = 0.26 +/- 0.05 for cells treated with 30 micro M CTB. These results provide the first quantitative assessment of the role that Pa-s-actin structure plays in the passive mechanical properties of human neutrophils.
肌动蛋白是真核细胞中一种普遍存在的蛋白质。它在细胞运动以及细胞形状的维持和控制中发挥着重要作用。在本文中，我们旨在探讨肌动蛋白对人类中性粒细胞被动力学特性的贡献。作为评估这种贡献的一个框架，中性粒细胞被模拟为具有恒定皮质（“表面”）张力的简单粘性液滴。使用试剂细胞松弛素B（CTB）破坏F - 肌动蛋白结构，并通过单细胞微量移液器抽吸来评估中性粒细胞的皮质张力和细胞质粘度。皮质张力通过简单的力平衡计算得出，粘度则根据细胞进入微量移液器的数值分析来计算。CTB以剂量依赖的方式降低细胞皮质张力：在3微摩尔浓度下降低19%，在30微摩尔浓度下降低49%。在相同的抽吸压力下比较时，CTB在3微摩尔浓度下还使细胞质粘度降低约25%，在30微摩尔浓度下降低约65%。所有三组中性粒细胞，即正常细胞以及用3或30微摩尔CTB处理的细胞，都表现出非牛顿行为，即表观粘度随剪切速率增加而降低。细胞质粘度对变形速率的依赖性可以通过经验公式μ = μc(γm/γc)-b来描述，其中μ是细胞质粘度，γm是平均剪切速率，μc是特征剪切速率γc下的特征粘度，b是材料系数。CTB处理降低了细胞质粘度对剪切速率的依赖性。这通过材料系数的变化得以体现。当γc设定为1秒-1时，正常中性粒细胞的μc = 130±23帕·秒，b = 0.52±0.09，而用30微摩尔CTB处理的细胞的μc = 54±15帕·秒，b = 0.26±0.05。这些结果首次对肌动蛋白结构在人类中性粒细胞被动力学特性中所起的作用进行了定量评估。
