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Histamine effects on endothelial cell fibronectin interaction studied by atomic force microscopy.
Andreea Trache1, Jerome P Trzeciakowski, Lesley Gardiner
1Department of Medical Physiology, Cardiovascular Research Institute, Texas A&M University System, College Station, TX 77843-1114, USA.
Biophysical Journal
|August 2, 2005
Summary
Histamine treatment increases endothelial cell stiffness and fibronectin-integrin binding strength, revealing its role in vascular leakage. Atomic force microscopy monitored these cellular changes, providing insights into inflammatory mediator effects.
Area of Science:
- Cell Biology
- Biophysics
- Biochemistry
Background:
- Histamine is a key inflammatory mediator.
- Histamine causes endothelial hyperpermeability and vascular leakage.
- Endothelial cell responses to inflammatory mediators involve cytoskeletal and adhesion dynamics.
Purpose of the Study:
- To investigate endothelial cell responses to histamine using atomic force microscopy (AFM).
- To measure the binding strength between alpha5beta1 integrin and fibronectin.
- To quantify changes in cell topography, stiffness, and adhesion force after histamine treatment.
Main Methods:
- Atomic force microscopy (AFM) with fibronectin-labeled probes.
- Measurement of single fibronectin-integrin bond rupture force.
- Monitoring of cell topography, local stiffness, and binding probability.
- Assessment of alpha5beta1-fibronectin interaction specificity using GRGDdSP.
Main Results:
- Histamine treatment induced endothelial cell shrinkage.
- Local cell stiffness and binding probability increased twofold post-histamine.
- The force to rupture single alpha5beta1-fibronectin bonds increased from 34.0 ± 0.5 pN to 39 ± 1 pN.
- GRGDdSP significantly reduced adhesion event probability but not adhesion force, confirming specificity.
Conclusions:
- Extracellular matrix-integrin interactions are crucial in the endothelial cell response to chemical mediators.
- AFM can directly measure these changes in live endothelial cells.
- Histamine modulates endothelial cell mechanics and integrin-ligand interactions, contributing to vascular leakage.