Journal
JOURNAL OF CELL SCIENCE
Volume 124, Issue 11, Pages 1936-1942Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.084657
Keywords
Actin cytoskeleton; Atomic force microscopy; Bis-oxonol; Cell stiffness; Electrical membrane potential; Endothelium
Categories
Funding
- Innovative Medizinische Forschung [OB510901, SH 510903]
- Deutsche Forschungsgemeinschaft [OB63/17-1, OB 63/18]
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The stiffness of vascular endothelial cells is crucial to mechanically withstand blood flow and, at the same time, to control deformation-dependent nitric oxide release. However, the regulation of mechanical stiffness is not yet understood. There is evidence that a possible regulator is the electrical plasma membrane potential difference. Using a novel technique that combines fluorescence-based membrane potential recordings with atomic force microscopy (AFM)-based stiffness measurements, the present study shows that membrane depolarization is associated with a decrease in the stiffness of endothelial cells. Three different depolarization protocols were applied, all of which led to a similar and significant decrease in cell stiffness, independently of changes in cell volume. Moreover, experiments using the actin-destabilizing agent cytochalasin D indicated that depolarization acts by affecting the cortical actin cytoskeleton. A model is proposed whereby a change of the electrical field across the plasma membrane is directly sensed by the submembranous actin network, regulating the actin polymerization: depolymerization ratio and thus cell stiffness. This depolarization-induced decrease in the stiffness of endothelial cells could play a role in flow-mediated nitric-oxide-dependent vasodilation.
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