Premium
Endothelial P‐selectin and vWf expressions are differentially regulated during high tidal volume ventilation
Author(s) -
Bhattacharya Sunita,
Yiming Maimaiti
Publication year - 2007
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.21.6.a1202-a
Subject(s) - von willebrand factor , platelet , p selectin , intracellular , chemistry , receptor , endocrinology , medicine , ventilation (architecture) , tidal volume , andrology , platelet activation , biology , biochemistry , respiratory system , mechanical engineering , engineering
Endothelial (EC) surface expressions of P‐selectin and von WIllebrand factor (vWf) underlie lung recruitment of leukocytes and platelets, respectively. We determined surface versus intracellular expressions, respectively in control and Triton‐permeabilized EC. From isolated blood‐perfused rat lungs (IBPLs) given 2 h of high (HV) or low (LV) tidal volume ventilation at 6 or 12 ml/kg, respectively, we recovered fresh EC (FLEC). We exposed FLEC to specific, fluorescence‐tagged mAbs, then viewed them by confocal microscopy. As compared with LV, HV increased surface P‐selectin and vWf by 98±8 and 69±8 %, respectively (mean±SE; n=3, P<.05). By contrast intracellular P‐selectin increased 89±8%, while vWf decreased 10±13% (n=3, P<.05). In HV, leukocyte‐ and platelet‐depleted blood perfusion decreased surface P‐selectin and vWf by 40±9 and 35±6% (n=3, P<.05), respectively and the corresponding stores by 22±2 and 25±6% (P<0.05). Thus in HV, stress‐induced increases of surface EC expression depleted intracellular stores of vWf, but not of P‐selectin. Leukocyte‐ and platelet‐depletion reduced store contents of both receptors equally. We conclude that ventilation stress differentially regulates EC stores by increasing P‐selectin and decreasing vWf. These differential effects are determined by EC interactions with leukocytes and platelets (Support: HL54157).