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- W94258972 abstract "We showed airway acid instillation caused lung endothelial (EC) protein tyrosine phosphorylation (Yiming, Faseb. J. 20: 2006). Here we addressed the underlying role of oxidative stress. We instilled normal saline (NS) or hydrochloric acid (HCI, pH1.2, 2ml/kg) in anesthetized mouse airway. 2 h later, injecting heparin, we cleared the pulmonary vasculature with ice-cold buffer, then perfused chilled collagenase (1000 units/ml) and trypsin (3ml) (Yiming, AJRCMB 2008), to obtain an effluent containing ~4x104 EC. Using fluorophore-conjugated mAbs, we surface labeled EC for the EC marker vWf or in fixed and permeabilized EC (paraformaldehyde, 2%, triton 0.1%) labeled vWf and phosphorylated tyrosine. We determined fluorescence by flow cytometry. As compared with saline, acid instillation markedly increased EC surface vWf and EC tyrosine phosphorylation (p<0.05, n=3). However, in the oxidant-incompetent gp91phox-/- mouse, acid-mediated vWf expression and tyrosine phosphorylation were markedly blunted (p<0.05, n=3). Taken together, our findings in wild type and gp91phox-/- mouse indicate oxidant stress promotes airway acid instillation-induced EC tyrosine kinase activation and platelet adherence molecule expression. We suggest that acute lung injury in acid aspiration results from an oxidant-induced platelet-adhesive endothelial surface (Support: HL36024)." @default.
- W94258972 created "2016-06-24" @default.
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- W94258972 date "2009-04-01" @default.
- W94258972 modified "2023-10-03" @default.
- W94258972 title "Airway acid instillation promotes procoagulant lung endothelial mechanisms in mouse" @default.
- W94258972 doi "https://doi.org/10.1096/fasebj.23.1_supplement.1023.5" @default.
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