Goldmann W H, Galneder R, Ludwig M, Kromm A, Ezzell R M
Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129, USA.
FEBS Lett. 1998 Mar 13;424(3):139-42. doi: 10.1016/s0014-5793(98)00155-0.
We studied the elasticity of both a wild type (F9) mouse embryonic carcinoma and a vinculin-deficient (5.51) cell line, which was produced by chemical mutagenesis. Using cell poking, we measured the effects of loss of vinculin on the elastic properties of these cells. F9 cells were about 20% more resistant to indentation by the cell poker (a glass stylus) than were 5.51 cells. Using the atomic force microscope to map the elasticity of wild type and vinculin-deficient cells by 128 X 128 force scans, we observed a correlation of elasticity with cell poking elastometric measurements. These findings, as well as previous atomic force, rheologic, and magnetometric measurements [Goldmann and Ezzell, Exp. Cell Res. 226 (1996) 234-237; Ezzell et al., Exp. Cell Res. 231 (1997) 14-26], indicate that vinculin is an integral part of the cytoskeletal network.
我们研究了野生型（F9）小鼠胚胎癌细胞系和通过化学诱变产生的纽蛋白缺陷型（5.51）细胞系的弹性。我们采用细胞针刺法，测量了纽蛋白缺失对这些细胞弹性特性的影响。与5.51细胞相比，F9细胞对细胞针刺器（玻璃探针）压痕的抵抗力约高20%。利用原子力显微镜通过128×128力扫描绘制野生型和纽蛋白缺陷型细胞的弹性图谱，我们观察到弹性与细胞针刺弹性测量之间的相关性。这些发现，以及之前的原子力、流变学和磁力测量结果[戈德曼和埃泽尔，《实验细胞研究》226（1996）234 - 237；埃泽尔等人，《实验细胞研究》231（1997）14 - 26]表明，纽蛋白是细胞骨架网络的一个组成部分。
