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).