Eckes B, Dogic D, Colucci-Guyon E, Wang N, Maniotis A, Ingber D, Merckling A, Langa F, Aumailley M, Delouvée A, Koteliansky V, Babinet C, Krieg T
Department of Dermatology, University of Cologne, Federal Republic of Germany.
J Cell Sci. 1998 Jul;111 ( Pt 13):1897-907. doi: 10.1242/jcs.111.13.1897.
Loss of a vimentin network due to gene disruption created viable mice that did not differ overtly from wild-type littermates. Here, primary fibroblasts derived from vimentin-deficient (-/-) and wild-type (+/+) mouse embryos were cultured, and biological functions were studied in in vitro systems resembling stress situations. Stiffness of -/- fibroblasts was reduced by 40% in comparison to wild-type cells. Vimentin-deficient cells also displayed reduced mechanical stability, motility and directional migration towards different chemo-attractive stimuli. Reorganization of collagen fibrils and contraction of collagen lattices were severely impaired. The spatial organization of focal contact proteins, as well as actin microfilament organization was disturbed. Thus, absence of a vimentin filament network does not impair basic cellular functions needed for growth in culture, but cells are mechanically less stable, and we propose that therefore they are impaired in all functions depending upon mechanical stability.
由于基因破坏导致波形蛋白网络缺失,产生了存活的小鼠,这些小鼠与野生型同窝小鼠没有明显差异。在此,培养了源自波形蛋白缺陷型(-/-)和野生型(+/+)小鼠胚胎的原代成纤维细胞,并在类似于应激情况的体外系统中研究其生物学功能。与野生型细胞相比,-/-成纤维细胞的硬度降低了40%。波形蛋白缺陷型细胞还表现出机械稳定性、运动性以及对不同化学吸引刺激的定向迁移能力降低。胶原纤维的重组和胶原晶格的收缩受到严重损害。粘着斑蛋白的空间组织以及肌动蛋白微丝组织受到干扰。因此,波形蛋白丝网络的缺失并不损害培养中生长所需的基本细胞功能,但细胞的机械稳定性较差,我们认为因此它们在所有依赖机械稳定性的功能中都受到损害。