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Fibroblasts probe substrate rigidity with filopodia extensions before occupying an area
Stephanie Wong1, Wei-Hui Guo1, Yu-Li Wang2
1Department of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, PA 15219.
Summary
Cells sense substrate rigidity using filopodia extensions to guide migration, preferring rigid surfaces for efficient movement and wound healing. This myosin II-driven mechanism probes ahead of the cell to avoid backtracking.
Area of Science:
- Cell biology
- Biophysics
- Mechanobiology
Background:
- Rigidity sensing and durotaxis are crucial for wound healing, tissue formation, and cancer.
- Studying cellular responses to rigidity interfaces is challenging due to transient cell behavior.
Purpose of the Study:
- To develop a model experimental system for studying cell responses to rigidity interfaces.
- To investigate the mechanisms of cell probing and spreading at rigidity borders.
Main Methods:
- Developed a micropatterned system with rigid and soft adhesive domains.
- Observed NIH 3T3 cell behavior and filopodia extensions at the rigidity border.
- Analyzed the role of myosin II in cell response to substrate rigidity.
Main Results:
- Cells exhibited a preference for rigid substrates, similar to conventional interfaces.
- Filopodia probed substrate rigidity ahead of the leading edge.
- Soft substrates inhibited focal adhesion maturation and promoted retraction; rigid substrates promoted spreading.
- Myosin II was essential for probing forces and retraction responses.
Conclusions:
- A myosin II-driven, filopodia-based mechanism enables cells to sense physical characteristics ahead of the leading edge.
- This sensing mechanism facilitates efficient cell migration and prevents backtracking on substrates.
- The findings offer insights into cell migration dynamics in developmental and disease contexts.
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