| First Author | Yiming MT | Year | 2008 |
| Journal | Am J Respir Cell Mol Biol | Volume | 39 |
| Issue | 5 | Pages | 569-75 |
| PubMed ID | 18483418 | Mgi Jnum | J:154277 |
| Mgi Id | MGI:4367559 | Doi | 10.1165/rcmb.2007-0332OC |
| Citation | Yiming MT, et al. (2008) Platelets enhance endothelial adhesiveness in high tidal volume ventilation. Am J Respir Cell Mol Biol 39(5):569-75 |
| abstractText | Although platelets induce lung inflammation, leading to acute lung injury (ALI), the extent of platelet-endothelial cell (EC) interactions remains poorly understood. Here, in a ventilation-stress model of lung inflammation, we show that platelet-EC interactions are important. We obtained freshly isolated lung endothelial cells (FLECs) from isolated, blood-perfused rat lungs exposed to ventilation at low tidal volume (LV) or stress-inducing high tidal volume (HV). Immunofluorescence and immunoprecipitation studies revealed HV-induced increases in cell-surface von Willebrand factor (vWf) expression on FLEC. This increased expression was inhibited by platelet removal from the lung perfusion and by including a P-selectin-blocking antibody in the lung perfusion. The expression was also blocked in lungs from P-selectin knockout (P sel(-/-)) mice perfused with autologous blood, but not with heterologous wild-type blood containing P-selectin-expressing platelets. These findings indicate that in ventilation stress, platelets transfer vWf to the EC surface and that platelet P-selectin plays a critical role in this transfer. Further evidence for such intercellular transfers was the HV-induced FLEC expressions of platelet glycoprotein 1b and of platelet P-selectin. We conclude that in ventilation stress, platelets deposit leukocyte- and platelet-binding proteins on the EC surface, thereby establishing the proinflammatory phenotype of the vascular lining. |
