Key result
Sidestream cigarette smoke increased endothelial permeability by stimulating p38 MAPK and myosin light chain phosphorylation, which was prevented by p38 MAPK inhibition and resveratrol.
Why the study?
Does p38 MAPK inhibition prevent sidestream cigarette smoke-induced endothelial permeability in human pulmonary artery endothelial cells?
Population
Human pulmonary artery endothelial cells (HPAEs) at passages 5-8
Comparison
Sidestream cigarette smoke extract, p38 MAPK… vs PBS control or inactive control SB202474 (2.5 µM)
Design
Preclinical
Authors
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p38 MAPK inhibition shows no clinical role in smokers yet; leaves open translation of endothelial protection to human vascular outcomes.
Does p38 MAPK inhibition prevent sidestream cigarette smoke-induced endothelial permeability in human pulmonary artery endothelial cells?
p-value: p=<0.05
p38 MAPK mediates sidestream cigarette smoke-induced endothelial permeability, and its inhibition protects endothelial barrier function in vitro.
Low et al. (2007) studied Endothelial permeability. Sidestream cigarette smoke (SCS) extract vs. PBS (Control) was evaluated on Transendothelial electrical resistance (TER) (p=<0.05). Sidestream cigarette smoke increased endothelial permeability by stimulating p38 MAPK and myosin light chain phosphorylation, which was prevented by p38 MAPK inhibition and resveratrol.
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