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Blood, 1 February 2001, Vol. 97, No. 3, pp. 692-699
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Oncostatin M promotes biphasic tissue factor expression in smooth
muscle cells: evidence for Erk-1/2 activation
Toshiya Nishibe,
Graham Parry,
Atsushi Ishida,
Salim Aziz,
Jacqueline Murray,
Yatin Patel,
Salman Rahman,
Kurt Strand,
Keiko Saito,
Yuji Saito,
William P. Hammond,
Geoffrey F. Savidge,
Nigel Mackman, and
Errol S. Wijelath
From the Department of Molecular Biology, The Hope
Heart Institute and Providence Medical Center, Seattle, WA;
Departments of Immunology and Vascular Biology, The Scripps
Research Institute, La Jolla, CA; Division of Cardiothoracic
Surgery, Health Science Center, University of Colorado, Denver, CO;
Coagulation Research Laboratory, Haemophilia Reference Centre,
GKT Medical School, St. Thomas Hospital, London, United Kingdom.
Tissue factor (TF), a transmembrane glycoprotein, initiates the
extrinsic coagulation cascade. TF is known to play a major role in
mediating thrombosis and thrombotic episodes associated with the
progression of atherosclerosis. Macrophages at inflammatory sites, such
as atherosclerotic lesions, release numerous cytokines that are capable
of modulating TF expression. This study examined the role of oncostatin
M (OSM), a macrophage/ T-lymphocyte-restricted cytokine, in the
expression of TF in vascular smooth muscle cells (SMCs). It is reported
here that OSM stimulated a biphasic and sustained pattern of TF
messenger RNA (mRNA). The effect of OSM on TF mRNA expression was
regulated at the transcriptional level as determined by nuclear
run-offs and transient transfection of a TF promoter-reporter gene
construct. OSM-induced TF expression was regulated primarily by the
transcription factor NF- B. Activation of NF-B by OSM did not
require IB- degradation. Inhibition of MEK activity by U0126
prevented OSM-induced TF expression by suppressing NF-B DNA binding
activity as determined by gel-shift analysis. Further, inhibition of
Erk-1/2 protein by antisense treatment resulted in suppression of TF
mRNA expression, indicating a role for Erk-1/2 in modulating NF-B
DNA binding activity. These studies suggest that the induced expression
of TF by OSM is primarily through the activation of NF-B and that
activation of NF-B is regulated in part by the MEK/Erk-1/2 signal
transduction pathway. This study indicates that OSM may play a key role
in promoting TF expression in SMCs within atherosclerotic lesions.
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