Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms15313
Keywords
-
Categories
Funding
- National Institutes of Health [RC1-CA-145044, R01-CA-172986, U54-CA-210190]
- National Science Foundation Graduate Research Fellowship [00006595]
- University of Minnesota Department of Chemical Engineering and Materials Science William F. Ranz Fellowship
- Bill and Triana Silliman Fellowship
- University of Minnesota Informatics Institute Updraft Fund
- University of Minnesota Institute for Engineering in Medicine
- University of Minnesota Undergraduate Research Opportunities Program
Ask authors/readers for more resources
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 similar to 1 kPa) and U251 glioma cells (optimum similar to 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available
Share Paper
