Tumor necrosis factor α-induced vascular leakage involves PECAM1 phosphorylation

Elisabetta Ferrero, Antonello Villa, Maria Elena Ferrero, Elisabetta Toninelli, Jeffrey R. Bender, Ruggero Pardi, Maria Raffaella Zocchi

Research output: Contribution to journalArticlepeer-review


Herein we show that exposure of human umbilical vein endothelial cells to tumor necrosis factor α (TNFα) led to platelet endothelial cell adhesion molecule-1 (PECAM1) surface redistribution, disruption of cytoskeleton connections, and increased PECAM1 phosphorylation, accompanied by increased permeability to macromolecules. The in vitro use of inhibitors of tyrosine or serine-threonine kinases could prevent both PECAM1 surface redistribution and the increase in permeability induced by the cytokine. In vivo administration of lavendustin A, a natural tyrosine kinase inhibitor, protected endothelial cells from TNFα-dependent vascular leakage in mouse liver. We propose that the involvement of PECAM1 in TNFα-mediated effects on vascular permeability may depend on a dynamically regulated cytoskeletal association, related to the degree of PECAM1 phosphorylation.

Original languageEnglish
Pages (from-to)3211-3215
Number of pages5
JournalCancer Research
Issue number14
Publication statusPublished - Jul 15 1996

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


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