PEG protects lung endothelial cells
The release of pro-inflammatory cytokines and extravasation of blood neutrophils into the bronchi may lead to tissue injury, particularly to airway epithelial cells and vascular endothelial cells. This causes an increase in the permeability of the microvascular membrane and the development of interstitial and alveolar protein-rich edema that hinders gas exchange and results in respiratory failure. Thus, therapeutic strategies that target vascular membrane integrity would have obvious clinical impact utility.
PEG has great potential in maintaining the integrity, or repairing lung endothelial cell (EC). Indeed, PEG induced rapid, dose-dependent augmentation in transendothelial electrical resistance (TER) in human pulmonary endothelium, reflecting increased paracellular integrity (Chiang et al., 2009). PEG also effectively reversed both thrombin and LPS-induced EC barrier dysfunction. PEG induced significant cytoskeletal rearrangement with the formation of well-defined cortical actin (Chiang et al., 2009). Consistent with this, Bejaoui et al have shown that PEG35 contributes to the regulation of endothelial cell barrier by rearranging the actin cytoskeleton (Bejaoui et al., 2016). Moreover, it has been shown that PEG induced membrane stabilization through the preservation of sarcolemmal lipid-raft architecture (Malhotra et al., 2011). Also, PEG repairs neuronal membrane injury and enhances functional recovery by at least two different mechanisms: resealing of the disrupted membrane and direct protection of mitochondria (Shi, 2013).