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Does TNF-α directly increase endothelial cell monolayer permeability?

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Abstract

The effects of dexamethasone (DEX) and ϖ methyl ester (l-NAME) on the tumour necrosis factor-α (TNF-α)-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 (1μM, 2 h) completely abolished the effect of TNF-α (5 ng/ml, 18 h). Administration of DEX 2 h after TNF-α also reduced the effect of TNF-α, whilel-NAME (5 ng/ml, 1 mM, 18 h) had no significant effect.

The observed inhibition of the TNF-α-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 withl-NAME. The inhibition caused by DEX administered after TNF-α would suggest alternative mechanisms by which DEX may be acting in addition to inhibition of NO synthase induction.

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Authors and Affiliations

  1. Children's Research Centre, Our Lady's Hospital for Sick Children, Crumlin, Dublin 12

    A. Burke-Gaffney

  2. Department for Pharmacology, University College Dublin, Belfield, Dublin 4, Ireland

    A. Burke-Gaffney & A. K. Keenan

Authors
  1. A. Burke-Gaffney
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  2. A. K. Keenan
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Burke-Gaffney, A., Keenan, A.K. Does TNF-α directly increase endothelial cell monolayer permeability?. Agents and Actions 38 (Suppl 2), C83–C85 (1993). https://doi.org/10.1007/BF01991145

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  • DOI: https://doi.org/10.1007/BF01991145

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