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Rigidity sensing and adaptation through regulation of integrin types
Alberto Elosegui-Artola1, Elsa Bazellières2, Michael D Allen3
11] Centre for Tumour Biology Barts Cancer Institute-a Cancer Research UK Centre of Excellence, Queen Mary, University of London, London EC1M 6BQ, UK [2] Institute for Bioengineering of Catalonia, 08028 Barcelona, Spain.
Nature Materials
|May 6, 2014
Summary
Cellular sensing of tissue rigidity depends on integrin bond dynamics. Different integrin types (α5β1 and αvβ6) adapt cell behavior to varying matrix stiffness, impacting development and cancer progression.
Area of Science:
- Cell Biology
- Biophysics
- Biochemistry
Background:
- Tissue rigidity is a critical regulator of cellular processes, including development, cancer progression, and wound healing.
- The mechanisms by which cells detect and respond to matrix stiffness remain largely unexplored.
Purpose of the Study:
- To elucidate how breast myoepithelial cells sense and adapt to varying matrix rigidity.
- To investigate the role of integrin bond dynamics in mediating cellular responses to tissue stiffness.
Main Methods:
- In vitro cell binding assays using fibronectin.
- Analysis of integrin (α5β1 and αvβ6) bond dynamics, including binding and unbinding rates.
- Theoretical modeling to explain observed cellular behaviors.
- Measurements of force generation, actin flow, and integrin recruitment.
Main Results:
- Integrin bond dynamics, specifically the rates of binding and unbinding to fibronectin, determine cellular adaptation to matrix rigidity.
- α5β1 integrins mediate adaptation to healthy tissue rigidity, while αvβ6 integrins mediate adaptation to malignant tissue rigidity.
- This integrin-mediated rigidity sensing is effective even when integrins compete for binding.
Conclusions:
- Integrin type and its specific bond dynamics are key determinants of cellular rigidity sensing.
- Differential integrin engagement allows cells to modulate behavior in response to distinct tissue stiffness, relevant to cancer and development.
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