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J Biol Chem, Vol. 274, Issue 52, 37362-37369, December 24, 1999
From the Cardiac chamber morphogenesis requires the
coordinated growth of both cardiac muscle and endocardial cell
lineages. Paracrine growth factors may modulate the coordinated
cellular specification and differentiation during cardiac chamber
morphogenesis, as suggested by the essential role of
endothelial-derived growth factors, neuregulin-1, and insulin-like
growth factor-I. Using the whole mouse embryo culture system for
delivery of diffusible factors into the cardiac chamber, neuregulin-1
was shown to promote trabeculation of the ventricular wall. Another
factor, insulin-like growth factor-I, had no apparent effect by itself.
Combined treatment with neuregulin-1 and insulin-like growth factor-I
strongly induced DNA synthesis of cardiomyocytes and expansion of both
the ventricular compact zone and the atrioventricular cushions leading
to chamber growth and maturation. In cultured cardiomyocytes,
combined neuregulin-1 and insulin-like growth factor-I also had a
synergistic effect to promote DNA synthesis and cellular growth, which
were prevented by wortmannin, an inhibitor of phosphatidylinositol
3-kinase. Adenoviral delivery of dominant negative Rac1, which acts
downstream of phosphatidylinositol 3-kinase, blocked the effect of
combined neuregulin-1/insulin-like growth factor-I treatment. These
studies support the concept that the interaction of neuregulin-1 and
insulin-like growth factor-I pathways plays an important role in
coordinating cardiac chamber morphogenesis and may occur through
convergent activation of phosphatidylinositol 3-kinase.
Synergistic Roles of Neuregulin-1 and Insulin-like Growth
Factor-I in Activation of the Phosphatidylinositol 3-Kinase Pathway and
Cardiac Chamber Morphogenesis*
,
University of California, San Diego/Salk
Program in Molecular Medicine, Department of Medicine and Center for
Molecular Genetics, University of California, San Diego, La Jolla,
California 92093-0613, the § Department of Cell Biology and
Anatomy, Medical University of South Carolina, Charleston, South
Carolina 29425-2204, and the ¶ Department of Physiology,
University of Maryland, Baltimore, Maryland 20212
*
This work was supported by grants from the National
Institutes of Health (to K. R. C.).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: Dept. of Medicine,
0613-C, University of California, San Diego, 9500 Gilman Dr., La Jolla,
CA 92093-0613. Tel.: 619-534-6835; Fax: 619-534-8180; E-mail:
kchien@ucsd.edu.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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