ArticleThe Journal of clinical investigation1991
Adenosine diphosphate-ribosylation of G-actin by botulinum C2 toxin increases endothelial permeability in vitro.
Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 68 citations in OpenAlex.
- A Facile Method to Probe the Vascular Permeability of Nanoparticles in Nanomedicine Applications.Scientific reports · 2017Article
- Dynamics of pulmonary endothelial barrier function in acute inflammation: mechanisms and therapeutic perspectives.Cell and tissue research · 2014Review
- Article
- Binary bacterial toxins: biochemistry, biology, and applications of common Clostridium and Bacillus proteins.Microbiology and molecular biology reviews : MMBR · 2004Review
- Cytoskeletal alterations in lipopolysaccharide-induced bovine vascular endothelial cell injury and its prevention by sodium arsenite.Clinical and diagnostic laboratory immunology · 2000Article
- Barrier effects of hyperosmolar signaling in microvascular endothelium of rat lung.The Journal of clinical investigation · 1997Article
- Microinjection of ADP-ribosylated actin inhibits actin synthesis in hepatocyte-hepatoma hybrid cells.The Biochemical journal · 1996Article
- Article
- Effect of disruption of actin filaments by Clostridium botulinum C2 toxin on insulin secretion in HIT-T15 cells and pancreatic islets.Molecular biology of the cell · 1994Article
- Clostridial ADP-ribosylating toxins: effects on ATP and GTP-binding proteins.Molecular and cellular biochemistry · 1994Review
- Modulation of endothelial cell permeability by lung carcinoma cells: a potential mechanism of malignant pleural effusion formation.Inflammation · 1994Article
- SPARC (secreted protein acidic and rich in cysteine) regulates endothelial cell shape and barrier function.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- Disruption of cytoskeletal structures mediates shear stress-induced endothelin-1 gene expression in cultured porcine aortic endothelial cells.The Journal of clinical investigation · 1993Article
- Pore-forming bacterial toxins potently induce release of nitric oxide in porcine endothelial cells.The Journal of experimental medicine · 1993Article
- Role of phosphodiesterases in the regulation of endothelial permeability in vitro.The Journal of clinical investigation · 1993Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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