Advertisement

Research Article Free access | 10.1172/JCI115171

Adenosine diphosphate-ribosylation of G-actin by botulinum C2 toxin increases endothelial permeability in vitro.

N Suttorp, M Polley, J Seybold, H Schnittler, W Seeger, F Grimminger, and K Aktories

Department of Internal Medicine, Justus Liebig-University, Giessen, Germany.

Find articles by Suttorp, N. in: PubMed | Google Scholar

Department of Internal Medicine, Justus Liebig-University, Giessen, Germany.

Find articles by Polley, M. in: PubMed | Google Scholar

Department of Internal Medicine, Justus Liebig-University, Giessen, Germany.

Find articles by Seybold, J. in: PubMed | Google Scholar

Department of Internal Medicine, Justus Liebig-University, Giessen, Germany.

Find articles by Schnittler, H. in: PubMed | Google Scholar

Department of Internal Medicine, Justus Liebig-University, Giessen, Germany.

Find articles by Seeger, W. in: PubMed | Google Scholar

Department of Internal Medicine, Justus Liebig-University, Giessen, Germany.

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

Department of Internal Medicine, Justus Liebig-University, Giessen, Germany.

Find articles by Aktories, K. in: PubMed | Google Scholar

Published May 1, 1991 - More info

Published in Volume 87, Issue 5 on May 1, 1991
J Clin Invest. 1991;87(5):1575–1584. https://doi.org/10.1172/JCI115171.
© 1991 The American Society for Clinical Investigation
Published May 1, 1991 - Version history
View PDF
Abstract

The endothelial cytoskeleton is believed to play an important role in the regulation of endothelial permeability. We used botulinum C2 toxin to perturb cellular actin and determined its effect on the permeability of endothelial cell monolayers derived from porcine pulmonary arteries. The substrate for botulinum C2 toxin is nonmuscle monomeric actin which becomes ADP-ribosylated. This modified actin cannot participate in actin polymerization and, in addition, acts as a capping protein. Exposure of endothelial cell monolayers to botulinum C2 toxin resulted in a dose- (3-100 ng/ml) and time-dependent (30-120 min) increase in the hydraulic conductivity and decrease in the selectivity of the cell monolayers. The effects of C2 toxin were accompanied by a time- and dose-dependent increase in ADP-ribosylatin of G-actin. G-Actin content increased and F-actin content decreased time- and dose-dependently in C2 toxin-treated endothelial cells. Phalloidin which stabilizes filamentous actin prevented the effects of botulinum C2 toxin on endothelial permeability. Botulinum C2 toxin induced interendothelial gaps. The effects occurred in the absence of overt cell damage and were not reversible within 2 h. The data suggest that the endothelial microfilament system is important for the regulation of endothelial permeability.

Images.

Browse pages

Click on an image below to see the page. View PDF of the complete article

Version history
  • Version 1 (May 1, 1991): No description
Advertisement
Advertisement