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Lung platelet‐endothelial interactions in high tidal volume ventilation
Author(s) -
Yiming Maimaiti T.,
Bhattacharya Sunita
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1178.19
Subject(s) - platelet , p selectin , lung , platelet activation , tidal volume , receptor , chemistry , von willebrand factor , endocrinology , medicine , andrology , immunology , microbiology and biotechnology , biology , respiratory system
Platelets amplify endothelial P‐selectin expression in high tidal volume ventilation (AJRCMB, 2005, 33:549‐54) but mechanisms underlying platelet‐endothelial interactions are not known. We considered the roles of the platelet inflammatory proteins, glycoprotein 1b alpha (GP1b‐α), vWf and P‐selectin. We recovered lung endothelial cells (FLEC) from freshly excised (control), or isolated, blood‐perfused rat lungs that we ventilated at tidal volume of 12 ml/kg for 2h (HV). Confocal microscopy of immunofluorescently labelled FLEC revealed that GP1b‐α and vWf were weakly expressed for control, but strongly expressed and colocalized for HV. Lung perfusion with the P‐selectin function‐blocking mAb, RMP‐1 markedly inhibited the HV‐induced vWf expression (P<0.05). In contrast to WT, HV failed to increase vWf expression in FLEC from P‐selectin knockout (P‐sel −/− ) mice. This inhibitory effect was rescued by perfusing P‐sel −/− lungs with WT blood. We conclude that in HV, platelets transfer GP1b‐αto lung EC and that platelet P‐selectin determines EC vWf expression. Lung recruitment of inflammatory cells might result from platelet‐EC transfer of critical inflammatory receptors (Support: HL54157).