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Human endothelial cells are target for platelet-activating factor. I. Platelet-activating factor induces changes in
F Bussolino1, G Camussi, M Aglietta
1Dipartimento di Genetica, Biologia e Chimica Medica, Universita di Torino, Italy.
Journal of Immunology (Baltimore, Md. : 1950)
|October 1, 1987
Summary
Platelet-activating factor (PAF) alters human endothelial cell shape and promotes a migratory phenotype by affecting the cytoskeleton. PAF also increases vascular permeability, effects blocked by specific PAF-receptor antagonists.
Area of Science:
- Cell Biology
- Biochemistry
- Physiology
Background:
- Platelet-activating factor (PAF) is a potent lipid mediator involved in inflammation and immune responses.
- Endothelial cells (EC) form the inner lining of blood vessels and play a crucial role in regulating vascular permeability.
Purpose of the Study:
- To investigate the effects of Platelet-activating factor (PAF) on human endothelial cell (EC) morphology and function.
- To elucidate the underlying mechanisms of PAF-induced changes in EC, including cytoskeletal alterations and vascular permeability.
Main Methods:
- Human endothelial cells (EC) in culture were treated with varying concentrations of PAF and lyso-PAF.
- Cell morphology, stress fiber distribution, and vinculin localization were analyzed using microscopy.
- F-actin content was quantified via phalloidin staining and fluorescence measurement.
- Vascular permeability was assessed by measuring 125I-albumin diffusion across EC monolayers.
- The effects of four distinct PAF-receptor antagonists were evaluated.
Main Results:
- PAF, but not lyso-PAF, induced dose-dependent changes in EC shape, leading to retraction and a migratory phenotype.
- PAF treatment resulted in altered stress fiber organization and a diffuse distribution of vinculin.
- PAF significantly reduced F-actin content in EC in a time- and concentration-dependent manner.
- PAF increased 125I-albumin diffusion across EC monolayers, indicating increased vascular permeability.
- Four different PAF-receptor antagonists effectively blocked PAF-induced alterations in EC.
Conclusions:
- PAF induces significant cytoskeletal rearrangements and a migratory phenotype in human endothelial cells.
- PAF increases vascular permeability, likely through mechanisms involving cytoskeletal changes and F-actin depolymerization.
- The observed effects are mediated by a specific PAF receptor, as evidenced by the action of receptor antagonists.