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Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
Published on: August 13, 2015
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Modulation of monocyte-endothelial cell interactions by platelet microparticles
O P Barry1, D Praticò, R C Savani
1Center for Experimental Therapeutics, Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6100, USA.
The Journal of Clinical Investigation
|July 3, 1998
Summary
Platelet microparticles (MP) enhance monocyte adhesion to endothelial cells and promote monocyte migration. This interaction, mediated by arachidonic acid and protein kinase C, suggests a role for MP in atherosclerosis and inflammation.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Immunology
Background:
- Platelets release microparticles (MP) upon activation, but their biological roles are not fully understood.
- Platelet-derived MP have been shown to influence platelet and endothelial cell functions.
- The specific mechanisms by which MP mediate cellular activation require further investigation.
Purpose of the Study:
- To investigate the mechanism of cellular activation by platelet-derived MP.
- To examine the effects of platelet MP on monocyte-endothelial cell interactions in vitro.
- To determine if platelet MP influence monocyte adhesion and chemotaxis.
Main Methods:
- In vitro adhesion assays using human umbilical vein endothelial cells (HUVEC) and U-937 cells (monocyte model).
- Dose- and time-dependent analysis of MP effects on cellular adhesion and chemotaxis.
- Analysis of cell adhesion molecule expression (ICAM-1, VCAM-1, selectins, integrins) following MP stimulation.
- Investigation of the role of arachidonic acid and protein kinase C (PKC) using isolated arachidonic acid and a PKC inhibitor (GF 109203X).
Main Results:
- Platelet MP significantly increased monocyte and U-937 cell adhesion to HUVEC in a time- and dose-dependent manner.
- MP-induced adhesion was mimicked by arachidonic acid and involved upregulation of ICAM-1 on HUVEC and specific integrins on monocytes.
- Platelet MP also induced dose-dependent chemotaxis of U-937 cells, an effect mimicked by arachidonic acid.
- Protein kinase C (PKC) activation was implicated in both MP-induced adhesion and chemotaxis, as inhibition of PKC significantly reduced these responses.
Conclusions:
- Platelet-derived MP modulate key aspects of endothelial and monocyte function, including adhesion and chemotaxis.
- Arachidonic acid released from MP and protein kinase C signaling play crucial roles in mediating these effects.
- These findings suggest a novel mechanism for platelet interaction with monocytes and endothelial cells, potentially contributing to atherosclerosis and inflammation.
