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J. Biol. Chem., Vol. 276, Issue 44, 41143-41149, November 2, 2001
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From the ¶ Surgical Professorial Unit, St. Vincent's Hospital
and the Yin Yang-1 (YY1) is a multifunctional
transcription factor that can repress the expression of many growth
factor, hormone, and cytokine genes implicated in atherogenesis. YY1
expression is activated in rat vascular smooth muscle cells shortly
after injury. YY1 DNA binding activity paralleled elevated protein
levels in the nucleus. Smooth muscle cell injury triggered the rapid extracellular release of immunoreactive fibroblast growth factor-2 (FGF-2). YY1 induction after injury was blocked by neutralizing antibodies directed against FGF-2. This growth factor increased YY1
mRNA and protein expression and stimulated YY1 binding and transcriptional activity. Overexpression of YY1 inhibited smooth muscle
cell replication. Immunohistochemical analysis demonstrated YY1
staining in medial smooth muscle cells, coincident with FGF-2 expression. Proliferating cell nuclear antigen staining, in
contrast, was confined mainly to the atherosclerotic intima. This is
the first demonstration that YY1 is induced by either injury or FGF-2, is differentially expressed in normal and diseased human arteries, and
that its overexpression inhibits vascular smooth muscle but not
endothelial cell replication.
Induction of the Transcriptional Repressor Yin
Yang-1 by Vascular Cell Injury
AUTOCRINE/PARACRINE ROLE OF ENDOGENOUS FIBROBLAST GROWTH
FACTOR-2*
§,§,§
Center for Thrombosis and Vascular Research, The
University of New South Wales and the § Department of
Haematology, The Prince of Wales Hospital, Sydney, New South
Wales 2052, Australia
*
This work was supported in part by grants from the National
Heart Foundation of Australia, National Health and Medical Research Council (NHMRC) of Australia, and New South Wales State Department of
Health. H. C. L. was supported by a postgraduate medical research scholarship from the NHMRC. L. M. K. was supported by a research fellowship from the NHMRC of Australia.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Center for
Thrombosis and Vascular Research, School of Pathology, The University of New South Wales, Sydney, NSW 2052, Australia. Tel.: 61-2-9385-2537; Fax: 61-2-9385-1389; E-mail: L.Khachigian@unsw.edu.au.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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