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Integr Biol (Camb). 2015 Oct;7(10):1265-1271. doi: 10.1039/c5ib00080g. Epub 2015 Jul 6.

Single molecular force across single integrins dictates cell spreading.

Author information

1
Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801 USA.
2
Department of Physics and Center for Physics of Living Cells, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801 USA.
3
Howard Hughes Medical Institute, Urbana, IL 61801, USA.
4
Department of Mechanical Science and Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois, 61801 USA.
5
Department of Biomedical Engineering, School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.
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Contributed equally

Abstract

Cells' ability to sense and interpret mechanical signals from the extracellular milieu modulates the degree of cell spreading. Yet how cells detect such signals and activate downstream signaling at the molecular level remain elusive. Herein, we utilize tension gauge tether (TGT) platform to investigate the underlying molecular mechanism of cell spreading. Our data from both differentiated cells of cancerous and non-cancerous origin show that for the same stiff underlying glass substrates and for same ligand density it is the molecular forces across single integrins that ultimately determine cell spreading responses. Furthermore, by decoupling molecular stiffness and molecular tension we demonstrate that molecular stiffness has little influence on cell spreading. Our data provide strong evidence that links molecular forces at the cell-substrate interface to the degree of cell spreading.

PMID:
26143887
PMCID:
PMC4593737
DOI:
10.1039/c5ib00080g
[Indexed for MEDLINE]
Free PMC Article

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