Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
Arteriosclerosis, Thrombosis, and Vascular Biology. 1991;11:872-881

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Langeler, E. G.
Right arrow Articles by van Hinsbergh, V. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Langeler, E. G.
Right arrow Articles by van Hinsbergh, V. W.

Arteriosclerosis and Thrombosis, Vol 11, 872-881, Copyright © 1991 by American Heart Association


ARTICLES

Effects of tumor necrosis factor on prostacyclin production and the barrier function of human endothelial cell monolayers

EG Langeler, W Fiers and VW van Hinsbergh
Gaubius Institute, Leiden, The Netherlands.

The endothelium controls the influx of macromolecules into the tissues, a process that may be disturbed at sites of inflammation and in atherosclerotic plaques. In this article, we report our evaluations of the effects of the inflammatory mediator, tumor necrosis factor-alpha (TNF-alpha), on the production of prostacyclin and the barrier function of human endothelial cell monolayers in an in vitro model. TNF-alpha (500 units/ml) had no direct effect on the passage of sucrose, peroxidase, and low density lipoprotein through monolayers of human aortic endothelial cells. On the other hand, during the first hours after addition 500 units/ml TNF-alpha induced a reduction of the permeability of umbilical artery endothelial cell monolayers. Within 10 minutes TNF-alpha induced an increase in prostacyclin production by primary cultures of umbilical artery endothelial cells. However, the reduction in permeability was not caused by a change in prostacyclin production or by a change in cyclic AMP concentration because 1) the effect of TNF-alpha on permeability was not prevented by aspirin, 2) no change in the cellular cyclic AMP concentration could be observed after addition of TNF-alpha, and 3) TNF-alpha was still able to reduce the passage rate in the presence of 25 microM forskolin. The reduction in permeability was accompanied by a decrease of F-actin in stress fibers. With prolonged incubation with TNF-alpha, the permeability of umbilical artery endothelial cell monolayers increased, and F-actin was found again in stress fibers. However, these effects of TNF-alpha were only significant at high concentrations of TNF-alpha.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
M. W. Marino, J. D. Dunbar, L.-W. Wu, J. R. Ngaiza, H.-M. Han, D. Guo, M. Matsushita, A. C. Nairn, Y. Zhang, R. Kolesnick, et al.
Inhibition of Tumor Necrosis Factor Signal Transduction in Endothelial Cells by Dimethylaminopurine
J. Biol. Chem., November 8, 1996; 271(45): 28624 - 28629.
[Abstract] [Full Text] [PDF]