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Published on: September 27, 2012
Modification of Cellular Cholesterol Content Affects Traction Force, Adhesion and Cell Spreading
Leann L Norman1, Ratna J Oetama, Micah Dembo
1Fischell Department of Bioengineering, University of Maryland, College Park, MD 20742, USA.
Cellular and Molecular Bioengineering
|April 5, 2011
Summary
Cholesterol depletion increases cell stiffness by altering the actin cytoskeleton and plasma membrane interaction, leading to larger traction forces and focal adhesions. This highlights cholesterol's role in cell mechanics and adhesion.
Area of Science:
- Cell Biology
- Biophysics
- Biochemistry
Background:
- Cellular cholesterol is vital for plasma membrane physical properties like elasticity and permeability.
- Cholesterol depletion unexpectedly increases cell stiffness via actin cytoskeleton-plasma membrane interactions.
- This suggests increased traction stresses in the acto-myosin complex during cholesterol depletion.
Purpose of the Study:
- To quantify forces exerted by individual cells on a substrate using force traction microscopy.
- To observe cell-substrate adhesion and spreading using advanced microscopy techniques.
- To investigate the role of cholesterol in regulating cell-substrate interactions.
Main Methods:
- Force traction microscopy to measure cellular forces.
- Total internal reflection fluorescence microscopy for adhesion observation.
- Interference reflection microscopy for cell spreading analysis.
Main Results:
- Cholesterol-depleted cells exhibit larger traction forces and focal adhesions than untreated or enriched cells.
- Adhesion area decreases in cholesterol-depleted single cells and monolayers.
- Cholesterol-depleted cells show reduced spreading area, while enriched cells are unaffected.
Conclusions:
- Cholesterol regulates cell-substrate interactions through the actin-plasma membrane complex.
- Cholesterol influences cell-cell adhesion and cell spreading dynamics.
- These findings underscore cholesterol's critical role in cellular mechanical properties and adhesion.
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