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and TNF-
Induced Endothelial Cell Adhesion Molecule Expression and Resultant Adhesion
1 Chemical Engineering, Ohio University, Athens, OH, USA
* To whom correspondence should be addressed. E-mail: goetzd{at}ohio.edu.
A promising approach for reducing aberrant leukocyte-endothelial adhesion during pathological inflammation is to inhibit endothelial cell adhesion molecule (ECAM) expression at the transcription level. Several compounds have been shown to decrease cytokine-induced up-regulation of ECAMs primarily by modulating the activity of transcription factors (e.g. nuclear factor-
B (NF-B)). The majority of the in vitro studies have focused on the effect of transcription inhibitors on endothelial cells exposed to a single cytokine (primarily tumor necrosis factor-
(TNF-)) for a relatively short time period (primarily 4-6 hrs.). However, in the in vivo setting, multiple cytokines (e.g. interleukin-1
(IL-1) and TNF-) may be present for extended periods of time. Thus, we studied the effects of a transcription inhibitor, the proteasome inhibitor lactacystin, on ECAM expression and myeloid (HL60) cell adhesion to human umbilical vein endothelial cells (HUVEC) activated by concurrent, sequential and long term (24 hr.) treatment with IL-1 and TNF-. We show, for the first time, that lactacystin inhibits (i) 4 hr. concurrent IL-1 and TNF- induced expression of E-selectin, VCAM-1, ICAM-1 and HL60 cell adhesion to HUVEC, (ii) 4 hr. TNF- induced expression of E-selectin, VCAM-1 and HL60 cell adhesion to HUVEC that have become desensitized to IL-1 activation, (iii) 24 hr. TNF- induced expression of E-selectin and VCAM-1 but not ICAM-1 and (iv) 24 hr. TNF- induced HL60 cell adhesion to HUVEC. Combined, our results demonstrate that a proteasome inhibitor can reduce concurrent, sequential and long term IL-1 and TNF- induced ECAM expression and myeloid cell adhesion.
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