Shifting the optimal stiffness for cell migration

Benjamin L. Bangasser, Ghaidan A. Shamsan, Clarence E. Chan, Kwaku N. Opoku, Erkan Tüzel, Benjamin W. Schlichtmann, Jesse A. Kasim, Benjamin J. Fuller, Brannon R. McCullough, Steven S. Rosenfeld and David J. Odde ()
Additional contact information
Benjamin L. Bangasser: University of Minnesota
Ghaidan A. Shamsan: University of Minnesota
Clarence E. Chan: University of Minnesota
Kwaku N. Opoku: University of Minnesota
Erkan Tüzel: University of Minnesota
Benjamin W. Schlichtmann: University of Minnesota
Jesse A. Kasim: University of Minnesota
Benjamin J. Fuller: University of Minnesota
Brannon R. McCullough: University of Minnesota
Steven S. Rosenfeld: Brain Tumor and Neuro-Oncology Center, Cleveland Clinic
David J. Odde: University of Minnesota

Nature Communications, 2017, vol. 8, issue 1, 1-10

Abstract: Abstract Cell migration, which is central to many biological processes including wound healing and cancer progression, is sensitive to environmental stiffness, and many cell types exhibit a stiffness optimum, at which migration is maximal. Here we present a cell migration simulator that predicts a stiffness optimum that can be shifted by altering the number of active molecular motors and clutches. This prediction is verified experimentally by comparing cell traction and F-actin retrograde flow for two cell types with differing amounts of active motors and clutches: embryonic chick forebrain neurons (ECFNs; optimum ∼1 kPa) and U251 glioma cells (optimum ∼100 kPa). In addition, the model predicts, and experiments confirm, that the stiffness optimum of U251 glioma cell migration, morphology and F-actin retrograde flow rate can be shifted to lower stiffness by simultaneous drug inhibition of myosin II motors and integrin-mediated adhesions.

Date: 2017
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DOI: 10.1038/ncomms15313

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