Letters to the Editor |
Department of Morphology and Embryology, University of Ferrara, Italy
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
In their study published online in Arteriosclerosis, Thrombosis, and Vascular Biology, OBrien et al demonstrate that activated protein C (APC) decreases tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) expression in endothelial cells.1 Although the molecular mechanism by which APC decreases the expression of TRAIL mRNA and protein via an Egr-1/Erk-1/2 pathway appears convincing, much less clear is whether the downregulation of TRAIL reflects a physiological relevant decrease of surface TRAIL or TRAIL release by endothelial cells. In fact, we have never detected surface TRAIL by flow cytometry in human umbilical vein endothelial cells (HUVECs), cultured with or without TNF-
(Figure). On the other hand, surface TRAIL was easily detectable in other cell model systems, such as peripheral blood-derived adherent macrophages (Figure). Moreover, we were also unable to document in ELISA (R&D System) detectable release of soluble TRAIL by HUVECs treated or not with TNF-
(data not shown).
| |||||||||||
Because in their study O Brien et al used an ELISA approach to detect the TRAIL
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2008 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |