Abstract
Cell-generated traction forces induce integrin activation, leading to focal adhesion growth and cell spreading. It remains unknown, however, whether integrin activation feeds back to impact the generation of cytoskeletal tension. Here, we used elastomeric micropost arrays to measure cellular traction forces in wildtype and integrin-null cells. We report that activation of β1 but not β3 integrin, by either increasing density of immobilized fibronectin or treating with manganese, elicited fibroblast spreading and cytoskeletal tension. Furthermore, this force generation required Rho kinase and myosin activity. These findings suggest that integrin activation and cell traction forces comprise a bi-directional signaling unit of cell adhesion.
Copyright © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
-
Animals
-
Cell Adhesion
-
Cell Line
-
Cell Movement
-
Cytoskeleton / metabolism
-
Fibroblasts / cytology
-
Fibroblasts / metabolism*
-
Fibronectins / chemistry
-
Immobilized Proteins / chemistry
-
Integrin alpha5 / genetics
-
Integrin alpha5 / metabolism
-
Integrin beta1 / genetics
-
Integrin beta1 / metabolism*
-
Integrin beta3 / genetics
-
Integrin beta3 / metabolism*
-
Manganese / metabolism
-
Mechanotransduction, Cellular*
-
Mice
-
Myosins / genetics
-
Myosins / metabolism
-
RNA, Small Interfering / genetics
-
Surface Tension
-
Up-Regulation
-
rho-Associated Kinases / genetics
-
rho-Associated Kinases / metabolism
Substances
-
Fibronectins
-
Immobilized Proteins
-
Integrin alpha5
-
Integrin beta1
-
Integrin beta3
-
RNA, Small Interfering
-
Manganese
-
rho-Associated Kinases
-
Myosins