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(Received for publication, May 2, 1996, and in revised form, June 3, 1996)
From the Division of Cardiology, University of Texas Medical
Branch, Galveston, Texas 77555
Thrombin is a potent modulator of vascular tone
and vascular smooth muscle cell (VSMC) mitogenesis. Early studies from
other laboratories demonstrated that cyclic AMP (cAMP) antagonizes the
mitogenic effects of platelet-derived growth factor and epidermal
growth factor by inhibiting the extracellular signal-regulated protein
kinases (ERKs; p42, p44) group of mitogen-activated protein kinases
(MAPKs) in several cell types. This report examines the role of ERKs
and Jun N-terminal kinase 1 (JNK1) groups of mitogen-activated protein
kinases in thrombin-induced DNA synthesis in VSMCs using agents such as
forskolin and dibutyrylcyclic AMP that increase intracellular cAMP
levels. Both agents significantly inhibited thrombin-stimulated DNA
synthesis in VSMCs. These agents, however, had no effect on thrombin
induction of ERKs activation and c-Fos expression, suggesting
divergence of the latter two events from the growth-signaling events of
thrombin that are sensitive to inhibition by cAMP. Thrombin activated
JNK1 and induced c-Jun expression in VSMCs in a
time-dependent manner. In contrast to ERKs and c-Fos,
thrombin-induced JNK1 activation and c-Jun expression were sensitive to
inhibition by forskolin, suggesting an association of these events with
thrombin-stimulated growth in these cells. Thrombin also increased AP-1
activity, and this response was significantly blunted by forskolin.
Together, these results demonstrate a correlation between JNK1
activation and c-Jun expression by thrombin and their association with
the mitogenic signaling events of thrombin in VSMCs.
Volume 271, Number 34,
Issue of August 23, 1996
pp. 20805-20810
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
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