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Research Article Free access | 10.1172/JCI114663

Increased endothelial albumin permeability mediated by protein kinase C activation.

J J Lynch, T J Ferro, F A Blumenstock, A M Brockenauer, and A B Malik

Department of Medicine, Albany Medical College of Union University, New York 12208.

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Department of Medicine, Albany Medical College of Union University, New York 12208.

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Department of Medicine, Albany Medical College of Union University, New York 12208.

Find articles by Blumenstock, F. in: PubMed | Google Scholar

Department of Medicine, Albany Medical College of Union University, New York 12208.

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Department of Medicine, Albany Medical College of Union University, New York 12208.

Find articles by Malik, A. in: PubMed | Google Scholar

Published June 1, 1990 - More info

Published in Volume 85, Issue 6 on June 1, 1990
J Clin Invest. 1990;85(6):1991–1998. https://doi.org/10.1172/JCI114663.
© 1990 The American Society for Clinical Investigation
Published June 1, 1990 - Version history
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Abstract

We examined the effects of activation of endothelial protein kinase C (PKC) of the endothelial barrier function. Exposure of confluent bovine pulmonary artery endothelial cell monolayers to phorbol 12-myristate 13-acetate (PMA) resulted in concentration-dependent (10(-8)-10(-6) M) increases in PKC activity and in the transendothelial flux of 125I-albumin. Exposure of the endothelium to 1-oleoyl 2-acetyl glycerol (OAG) also increased the transendothelial flux of 125I-albumin in a concentration-dependent manner. Neither 4 alpha-phorbol didecanoate nor 1-mono-oleoyl glycerol, which do not activate PKC, altered permeability. The increase in 125I-albumin permeability induced by PMA was inhibited by 25 microM H7 (a PKC inhibitor), but not by the control compound HA1004 (25 microM). After 16 h of exposure to PMA, 125I-albumin permeability returned to baseline and a significant reduction in cytosolic PKC activity was noted. Further challenge with PMA at this time resulted in no significant increase in PKC activity indicating downregulation of the enzyme; moreover, this PMA challenge did not increase endothelial permeability. Exposure of endothelial monolayers to phospholipase C (PLC), which increases membrane phosphatidylinositide turnover, or to alpha-thrombin also induced concentration-dependent activation of PKC and increases in 125I-albumin endothelial permeability. The thrombin- and PLC-induced permeability increases were inhibited by H7, but not by HA1004. The activation of endothelial PKC directly by PMA or OAG and by PLC and alpha-thrombin increases the transendothelial albumin permeability, indicating that PKC activation is an important signal transduction pathway by which extracellular mediators increase endothelial macromolecular transport.

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