p38 mitogen-activated protein kinase mediates sidestream cigarette smoke-induced endothelial permeability

Brad Low, Mei Liang, Jian Fu

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


Second-hand smoke is associated with increased risk of cardiovascular diseases. So far, little is known about the signaling mechanisms of second-hand smoke-induced vascular dysfunction. Endothelial junctions are fundamental structures important for maintaining endothelial barrier function. Our study showed that sidestream cigarette smoke (SCS), a major component of second-hand smoke, was able to disrupt endothelial junctions and increase endothelial permeability. Sidestream cigarette smoke stimulated the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and myosin light chain (MLC). A selective inhibitor of p38 MAPK (SB203580) prevented SCS-induced loss of endothelial barrier integrity as evidenced by transendothelial resistance measurements. Resveratrol, an antioxidant that was able to inhibit SCS-induced p38 MAPK and MLC phosphorylation, also protected endothelial cells from the damage. Thus, p38 MAPK mediates SCS-induced endothelial permeability. Inhibition of p38 MAPK may have therapeutic potential for second-hand smoke-induced vascular injury.

Original languageEnglish
Pages (from-to)225-231
Number of pages7
JournalJournal of Pharmacological Sciences
Issue number3
StatePublished - 2007


  • Cigarette smoke
  • Endothelial permeability
  • Myosin light chain (MLC)
  • Rho kinase
  • p38 mitogen-activated protein kinase (MAPK)

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology


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