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Published on: June 11, 2015
Platelets enhance endothelial adhesiveness in high tidal volume ventilation
Maimaiti T Yiming1, David J Lederer, Li Sun
1Department of Pediatrics, College of Physicians and Surgeons, Columbia University and St Luke's-Roosevelt Hospital Center, New York, NY 10019, USA.
Summary
Platelets transfer proteins to lung endothelial cells during ventilation stress, contributing to inflammation and acute lung injury. Platelet P-selectin is crucial for this process, promoting a proinflammatory state.
Area of Science:
- Pulmonary Medicine
- Hematology
- Cell Biology
Background:
- Platelets contribute to lung inflammation and acute lung injury (ALI).
- The precise mechanisms of platelet-endothelial cell (EC) interactions in lung inflammation are not fully understood.
Purpose of the Study:
- To investigate the role of platelet-endothelial cell interactions in a ventilation-stress model of lung inflammation.
- To elucidate the molecular mechanisms underlying platelet-induced changes in lung endothelial cells.
Main Methods:
- Isolated rat lungs were subjected to low (LV) or high tidal volume (HV) ventilation.
- Freshly isolated lung endothelial cells (FLECs) were analyzed using immunofluorescence and immunoprecipitation.
- Experiments involved platelet removal, P-selectin blocking antibodies, and P-selectin knockout mice.
Main Results:
- High tidal volume (HV) ventilation increased cell-surface von Willebrand factor (vWf) expression on FLECs.
- This increase was dependent on platelets and platelet P-selectin.
- FLECs also showed increased expression of platelet glycoprotein 1b and P-selectin after HV ventilation.
Conclusions:
- Platelets transfer von Willebrand factor (vWf) to the endothelial cell surface during ventilation stress.
- Platelet P-selectin is critical for this vWf transfer.
- Platelets deposit leukocyte- and platelet-binding proteins on ECs, promoting a proinflammatory vascular lining phenotype relevant to acute lung injury.
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