Determining the mechanical properties of plectin in mouse myoblasts and keratinocytes

Journal article


Publication Details

Author(s): Bonakdar N, Schilling A, Spörrer M, Lennert P, Mainka A, Winter L, Walko G, Wiche G, Fabry B, Goldmann W
Journal: Experimental Cell Research
Publication year: 2015
Volume: 331
Journal issue: 2
Pages range: 331-7
ISSN: 0014-4827


Abstract


Plectin is the prototype of an intermediate filament (IF)-based cytolinker protein. It affects cells mechanically by interlinking and anchoring cytoskeletal filaments and acts as scaffolding and docking platform for signaling proteins to control cytoskeleton dynamics. The most common disease caused by mutations in the human plectin gene, epidermolysis bullosa simplex with muscular dystrophy (EBS-MD), is characterized by severe skin blistering and progressive muscular dystrophy. Therefore, we compared the biomechanical properties and the response to mechanical stress of murine plectin-deficient myoblasts and keratinocytes with wild-type cells. Using a cell stretching device, plectin-deficient myoblasts exhibited lower mechanical vulnerability upon external stress compared to wild-type cells, which we attributed to lower cellular pre-stress. Contrary to myoblasts, wild-type and plectin-deficient keratinocytes showed no significant differences. In magnetic tweezer measurements using fibronectin-coated paramagnetic beads, the stiffness of keratinocytes was higher than of myoblasts. Interestingly, cell stiffness, adhesion strength, and cytoskeletal dynamics were strikingly altered in plectin-deficient compared to wild-type myoblasts, whereas smaller differences were observed between plectin-deficient and wild-type keratinocytes, indicating that plectin might be more important for stabilizing cytoskeletal structures in myoblasts than in keratinocytes. Traction forces strongly correlated with the stiffness of plectin-deficient and wild-type myoblasts and keratinocytes. Contrary to that cell motility was comparable in plectin-deficient and wild-type myoblasts, but was significantly increased in plectin-deficient compared to wild-type keratinocytes. Thus, we postulate that the lack of plectin has divergent implications on biomechanical properties depending on the respective cell type.



FAU Authors / FAU Editors

Bonakdar, Nawid Dr.
Lehrstuhl für Biophysik
Fabry, Ben Prof. Dr.
Lehrstuhl für Biophysik
Goldmann, Wolfgang Prof.
Professur für Biomedizinische Physik
Spörrer, Marina
Professur für Biomedizinische Physik


External institutions with authors

Medizinische Universität Wien


How to cite

APA:
Bonakdar, N., Schilling, A., Spörrer, M., Lennert, P., Mainka, A., Winter, L.,... Goldmann, W. (2015). Determining the mechanical properties of plectin in mouse myoblasts and keratinocytes. Experimental Cell Research, 331(2), 331-7. https://dx.doi.org/10.1016/j.yexcr.2014.10.001

MLA:
Bonakdar, Nawid, et al. "Determining the mechanical properties of plectin in mouse myoblasts and keratinocytes." Experimental Cell Research 331.2 (2015): 331-7.

BibTeX: 

Last updated on 2019-20-07 at 07:16