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J Biol Chem, Vol. 273, Issue 38, 24932-24938, September 18, 1998
Platelet-derived Growth Factor-specific Regulation of the
JE Promoter in Rat Aortic Smooth Muscle Cells
Vladimir Y.
Bogdanov §,
Michael
Poon , and
Mark B.
Taubman
From the Cardiovascular Institute and Department of
Medicine and the § Brookdale Center for Molecular
Biology, Mount Sinai School of Medicine,
New York, New York 10029
JE is a member of the family of
"immediate early" genes induced by growth factors and cytokines.
JE encodes a low molecular weight secretory glycoprotein
analogous to the human monocyte chemoattractant protein, MCP-1. JE and
MCP-1 proteins are thought to play an important role in inflammation
and in the recruitment of monocyte/macrophages to the vessel wall
during the development of atherosclerosis. We have previously reported
that the induction of JE in rat aortic smooth muscle cells
(SMC) was specific to platelet-derived growth factor (PDGF) and was not
seen with other growth agonists. Using a luciferase reporter system and
transient transfection assays of rat aortic SMC, we now report the
identification of a region in the proximal rat JE promoter
that is responsive to PDGF but not to other growth factors (angiotensin
II and -thrombin) or cytokines (interleukin 1- and tumor necrosis
factor- ). The full response to PDGF (~6-fold) requires the
cooperative activity of two potentially novel cis-acting
elements, at positions 146 to 128 and 84 to 59. While each
element produces a different pattern in electrophoretic mobility shift
assays, they appear to bind the same PDGF-responsive species. Further
analysis of these regions should provide important insights into
PDGF-specific responses in vascular SMC.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 1998 by the American Society for Biochemistry and Molecular Biology.
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