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Substrate stress relaxation regulates cell spreading

Author

Listed:
  • Ovijit Chaudhuri

    (School of Engineering and Applied Sciences, Harvard University
    Wyss Institute for Biologically Inspired Engineering, Harvard University
    Stanford University)

  • Luo Gu

    (School of Engineering and Applied Sciences, Harvard University
    Wyss Institute for Biologically Inspired Engineering, Harvard University)

  • Max Darnell

    (School of Engineering and Applied Sciences, Harvard University
    Wyss Institute for Biologically Inspired Engineering, Harvard University)

  • Darinka Klumpers

    (School of Engineering and Applied Sciences, Harvard University
    Wyss Institute for Biologically Inspired Engineering, Harvard University
    Research Institute MOVE, VU University Medical Center)

  • Sidi A. Bencherif

    (School of Engineering and Applied Sciences, Harvard University
    Wyss Institute for Biologically Inspired Engineering, Harvard University)

  • James C. Weaver

    (Wyss Institute for Biologically Inspired Engineering, Harvard University)

  • Nathaniel Huebsch

    (School of Engineering and Applied Sciences, Harvard University
    Gladstone Institute of Cardiovascular Disease)

  • David J. Mooney

    (School of Engineering and Applied Sciences, Harvard University
    Wyss Institute for Biologically Inspired Engineering, Harvard University)

Abstract

Studies of cellular mechanotransduction have converged upon the idea that cells sense extracellular matrix (ECM) elasticity by gauging resistance to the traction forces they exert on the ECM. However, these studies typically utilize purely elastic materials as substrates, whereas physiological ECMs are viscoelastic, and exhibit stress relaxation, so that cellular traction forces exerted by cells remodel the ECM. Here we investigate the influence of ECM stress relaxation on cell behaviour through computational modelling and cellular experiments. Surprisingly, both our computational model and experiments find that spreading for cells cultured on soft substrates that exhibit stress relaxation is greater than cells spreading on elastic substrates of the same modulus, but similar to that of cells spreading on stiffer elastic substrates. These findings challenge the current view of how cells sense and respond to the ECM.

Suggested Citation

  • Ovijit Chaudhuri & Luo Gu & Max Darnell & Darinka Klumpers & Sidi A. Bencherif & James C. Weaver & Nathaniel Huebsch & David J. Mooney, 2015. "Substrate stress relaxation regulates cell spreading," Nature Communications, Nature, vol. 6(1), pages 1-7, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7365
    DOI: 10.1038/ncomms7365
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    1. Oluwamayokun Oshinowo & Renee Copeland & Anamika Patel & Nina Shaver & Meredith E. Fay & Rebecca Jeltuhin & Yijin Xiang & Christina Caruso & Adiya E. Otumala & Sarah Hernandez & Priscilla Delgado & Ga, 2024. "Autoantibodies immuno-mechanically modulate platelet contractile force and bleeding risk," Nature Communications, Nature, vol. 15(1), pages 1-15, December.

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