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PubMed · 7686326

Does TNF-alpha directly increase endothelial cell monolayer permeability?

A Burke-Gaffney·A K Keenan
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Abstract

The effects of dexamethasone (DEX) and N omega-nitro-L-arginine methyl ester (L-NAME) on the tumour necrosis factor-alpha (TNF-alpha)-induced increase in permeability of human umbilical vein endothelial cell (HUVEC) monolayer to [125I] labelled bovine serum albumin (BSA) were examined. Preincubation of HUVEC monolayers with DEX (1 microM, 2h) completely abolished the effect of TNF-alpha (5 ng/ml, 18 h). Administration of DEX 2 h after TNF-alpha also reduced the effect of TNF-alpha while L-NAME (5 ng/ml, 1 mM, 18 h) had no significant effect. The observed inhibition of the TNF-alpha-induced permeability increase on preincubation with DEX would suggest a role for nitric oxide (NO) in mediating the permeability response. However, this is not confirmed by the experiments with L-NAME. The inhibition caused by DEX administered after TNF-alpha would suggest alternative mechanisms by which DEX may be acting in addition to inhibition of NO synthase induction.

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Amino Acid OxidoreductasesEndothelium, VascularEnzyme InductionHumansNitric OxideNitric Oxide SynthaseUmbilical VeinsJournal Article

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A Burke-Gaffney, A K Keenan. 1993. Does TNF-alpha directly increase endothelial cell monolayer permeability?. https://doi.org/10.1007/bf01991145

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