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Differential regulation of vascular cell adhesion molecule-1 gene
transcription by tumor necrosis factor alpha and interleukin-1 alpha in
dermal microvascular endothelial cells
J Gille, RA Swerlick, TJ Lawley and SW Caughman
Emory Skin Diseases Research Center, Department of Dermatology, Emory
University School of Medicine, Atlanta, GA 30322, USA.
As part of the inflammatory response, the localization of leukocytes
depends to an important degree on cytokine-induced expression of vascular
cell adhesion molecule-1 (VCAM-1) on endothelial cells (EC). We have
previously shown that VCAM-1 expression is induced on human umbilical vein
EC (HUVEC) by both tumor necrosis factor alpha (TNF- alpha) and
interleukin-1 alpha (IL-1 alpha), whereas on human dermal microvascular EC
(HDMEC) only TNF alpha results in VCAM-1 expression. To explore molecular
mechanisms responsible for these contrasting patterns of VCAM-1 induction
in HUVEC versus HDMEC, we performed transcriptional activation studies with
VCAM-1-based reporter constructs and in vitro binding assays using two
adjacent NF-kappa B binding sequences of the VCAM-1 promoter as a DNA
probe. Previous studies have established that these NF-kappa B motifs are
required for cytokine-induced VCAM-1 transcription, and may further mediate
cell- specific VCAM-1 gene activation by cytokines. The findings reported
here demonstrate a significant HDMEC-specific attenuation of VCAM-1 gene
transcription in response to IL-1 alpha, but not TNF alpha. An upstream
VCAM-1 gene regulatory region distinct from the NF-kappa B sites appears to
function as an IL-1 alpha-mediated transcriptional repressor within HDMEC.
This repressor region conveys IL-1 alpha- dependent, but not TNF
alpha-dependent, inhibition of transcription driven by a heterologous
cytokine response element and promoter.
Volume 87,
Issue 1,
pp. 211-217,
01/01/1996
Copyright © 1996 by The American Society of Hematology
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