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10:31
Micropipette Aspiration of Substrate-attached Cells to Estimate Cell Stiffness
Published on: September 27, 2012
oxLDL-induced decrease in lipid order of membrane domains is inversely correlated with endothelial stiffness and
Tzu Pin Shentu1, Igor Titushkin, Dev K Singh
1Pulmonary, Critical Care and Sleep Medicine, Dept. of Medicine, University of Illinois, Chicago, Illinois 60612-7323, USA.
American Journal of Physiology. Cell Physiology
|April 23, 2010
Summary
Oxidized low-density lipoprotein (oxLDL) disrupts cell membrane lipid packing, increasing endothelial cell stiffness and impacting network formation. Cholesterol can reverse these atherosclerosis-linked effects.
Area of Science:
- Cardiovascular Biology
- Biophysics
- Cellular Mechanics
Background:
- Oxidized low-density lipoprotein (oxLDL) is a key factor in atherosclerosis development.
- Previous studies linked oxLDL to increased endothelial cell (EC) stiffness, force generation, and network formation.
Purpose of the Study:
- To investigate the molecular mechanisms by which oxLDL affects EC biomechanics and network formation.
- To explore the role of membrane lipid order in oxLDL-induced EC changes.
Main Methods:
- Laurdan two-photon imaging to assess membrane domain lipid packing.
- Atomic force microscopy to measure endothelial cell stiffness (elastic modulus).
- Assessment of cell contractility and EC angiogenic potential in 3D collagen gels.
Main Results:
- Oxidized low-density lipoprotein (oxLDL) decreases lipid order in membrane domains, inversely correlating with EC stiffness and network formation.
- Cholesterol supplementation fully reversed oxLDL-induced changes in EC biomechanics and network formation.
- 7-keto-cholesterol and androstenol also disrupted lipid order and increased EC stiffness.
Conclusions:
- Disruption of lipid packing in cholesterol-rich membrane domains is a key mechanism in oxLDL-induced endothelial cell biomechanical changes.
- Targeting membrane lipid order may offer therapeutic strategies for atherosclerosis.
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