p38 Mitogen-Activated Protein Kinase Mediates Sidestream Cigarette Smoke-Induced Endothelial Permeability

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概要

• 論文の詳細を見る

• 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.

• 社団法人 日本薬理学会の論文
• 2007-07-20

著者

• Low Brad

  Center For Biomedical Research University Of Texas Health Center At Tyler

• LIANG Mei

  Center for Biomedical Research, University of Texas Health Center at Tyler

• FU Jian

  Center for Biomedical Research, University of Texas Health Center at Tyler

• Fu Jian

  Center For Biomedical Research University Of Texas Health Center At Tyler

• Liang Mei

  Center For Biomedical Research University Of Texas Health Center At Tyler

関連論文

• Angiotensin II Directly Triggers Endothelial Exocytosis via Protein Kinase C-Dependent Protein Kinase D2 Activation
• p38 Mitogen-Activated Protein Kinase Mediates Sidestream Cigarette Smoke-Induced Endothelial Permeability

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