Impaired mechanical stability, migration and contractile capacity in vimentin-deficient fibroblasts

• Published in: Journal of cell science Vol. 111 ( Pt 13); no. 13; pp. 1897 - 1907
• Main Authors: Eckes, B., Dogic, D., Colucci-Guyon, E., Wang, N., Maniotis, A., Ingber, D., Merckling, A., Langa, F., Aumailley, M., Delouvee, A., Koteliansky, V., Babinet, C., Krieg, T.
• Format: Journal Article
• Language: English
• Published: Legacy CDMS 01.07.1998
• Subjects: Actins - metabolism; Animals; Cell Adhesion - genetics; Cell Movement - genetics; Cell Size - genetics; Cells, Cultured; Chemotaxis - genetics; Collagen - metabolism; Collagen - physiology; Fibroblasts - metabolism; Fibroblasts - pathology; Intercellular Junctions - genetics; Life Sciences (General); Mice; Mice, Knockout; Stress, Mechanical; Vimentin - deficiency; Vimentin - genetics; Non-Nasa Center; Nasa Discipline Cell Biology; NASA Discipline Cell Biology; Non-NASA Center
• ISSN: 0021-9533; 1477-9137
• 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.