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J Biol Chem, Vol. 273, Issue 13, 7725-7730, March 27, 1998
From the ¶ Department of Pharmacology and Graduate Program in
Biomedical Sciences and The assembly of contractile proteins into
organized sarcomeric units is one of the most distinctive features of
cardiac myocyte hypertrophy. In a well characterized in
vitro model system using cultured neonatal rat ventricular
myocytes, a subset of G protein-coupled receptor agonists has been
shown to induce actin-myosin filament organization. Pretreatment of
myocytes with C3 exoenzyme ADP-ribosylated Rho and inhibited the
characteristic
The Low Molecular Weight GTPase Rho Regulates Myofibril Formation
and Organization in Neonatal Rat Ventricular Myocytes
INVOLVEMENT OF Rho KINASE
,,, and Department of Medicine and Center
for Molecular Genetics, University of California, San Diego,
La Jolla, California 92093
1-adrenergic receptor agonist-induced myofibrillar organization, suggesting involvement of the Rho GTPase in
cardiac myofibrillogenesis. We used adenoviral mediated gene transfer
to examine the effects of activated Rho and inhibitory mutants of one
of its effectors, Rho kinase, in myocytes. Rho immunoreactivity was
increased in the particulate fraction of myocytes infected with a
recombinant adenovirus expressing constitutively activated Rho.
Rho-infected cells demonstrated a striking increase in the assembly and
organization of sarcomeric units and in the expression of the atrial
natriuretic factor protein. These Rho-induced responses were markedly
inhibited by co-infection with adenoviruses expressing putative
dominant negative forms of Rho kinase. A parallel pathway involving
Ras-induced myofibrillar organization and atrial natriuretic factor
expression was only minimally affected. 1-Adrenergic receptor agonist-induced myofibrillogenesis was inhibited by some but
not all of the Rho kinase mutants. Our data demonstrate that activated
Rho has profound effects on myofibrillar organization in cardiac
myocytes and suggest that Rho kinase mediates Rho-induced hypertrophic
responses.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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