Regulation of endothelial permeability by second messengers.
The mechanisms by which mediators such as oxidants released by neutrophil (PMN) activation increase endothelial permeability are poorly understood. The focus of this article is to identify some of these mechanisms. Studies using endothelial cell monolayers in culture have shown that PMN activation increases endothelial permeability both in the presence and absence of PMN-endothelial monolayer contact. Hydrogen peroxide (H2O2), an oxidant released by PMN activation, plays an important role in PMN-induced increases in endothelial permeability. The results of these studies suggest that, as with other mediators of inflammation (e.g., histamine, thrombin) the mechanism of H2O2-induced increase in endothelial permeability involves activation of endothelial protein kinase C (PKC) and increase in endothelial cytosolic Ca2+.
Siflinger-Birnboim
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A
Department of Physiology and Cell Biology (A134), Albany Medical College, NY 12208, USA.
Malik
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AB
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002199:Capillary Permeability / Q000187:drug effects / Q000502:physiology; D000242:Cyclic AMP / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000502:physiology*; D018375:Neutrophil Activation / Q000502:physiology*; D011493:Protein Kinase C / Q000378:metabolism; D015290:Second Messenger Systems / Q000502:physiology*
D018836:Inflammation Mediators; D006861:Hydrogen Peroxide; D000242:Cyclic AMP; D011493:Protein Kinase C; D002118:Calcium