Published online before print March 20, 2003, doi: 10.1161/01.RES.0000067928.83455.9C
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Submitted on August 15, 2002
Revised on March 11, 2003
Accepted on March 11, 2003
Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) Sequentially Upregulates Nitric Oxide and Prostanoid Production in Primary Human Endothelial Cells
Giorgio Zauli *;
From the Department of Normal Human Morphology (G.Z., M.V.), University of Trieste, Trieste, Italy; the Department of Biomorphology (A.P., R.D.P., R.R.), "G. D'Annunzio" University of Chieti, Chieti Scalo, Chieti, Italy; the Department of Morphology and Embryology (A.G., P.S.), Human Anatomy Section, University of Ferrara, Ferrara, Italy; and the Department of Drug Sciences (S.G., G.C.), "G. D'Annunzio" University of Chieti, Chieti, Italy.
* To whom correspondence should be addressed. E-mail: zauli{at}units.it.
Endothelial cells express tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors, but the function of TRAIL in endothelial cells is not completely understood. We explored the role of TRAIL in regulation of key intracellular signal pathways in endothelial cells. The addition of TRAIL to primary human endothelial cells increased phosphorylation of endothelial nitric oxide synthase (eNOS), NOS activity, and NO synthesis. Moreover, TRAIL induced cell migration and cytoskeleton reorganization in an NO-dependent manner. TRAIL did not activate the NF-
B or COX-2 pathways in endothelial cells. Instead, TRAIL increased prostanoid production (PGE2=PGI2>TXA2), which was preferentially inhibited by the COX-1 inhibitor SC-560. Because NO and prostanoids play a crucial role in the state of blood vessel vasodilatation and angiogenesis, our data suggest that TRAIL might play an important role in endothelial cell function.
Key words: tumor necrosis factor-related apoptosis-inducing ligand • nitric oxide • prostanoids
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