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Vol. 63, Issue 2, 368-377, February 2003
Jean Mayer United States Department of Agriculture Human Nutrition
Research Center on Aging (Y.K., A.-G.M., S.N.F., Y.J.S.) and Pulmonary
and Critical Care Division (A.R.S., Y.J.S.), Department of
Medicine, Tufts University, Boston, Massachusetts; Protein Science
Laboratory (K.K.), National Food Research Institute, Tsukuba, Japan;
Hokkaido Food Processing Research Center (T.I., Y.I.), Hokkaido, Japan;
and Department of Developmental and Molecular Biology (T.E.), Albert
Einstein College of Medicine, Bronx, New York
Anthracyclines are effective cancer chemotherapeutic agents but can
induce serious cardiotoxicity. Understanding the mechanism of cardiac
damage by these agents will help in development of better therapeutic
strategies against cancer. The GATA-4 transcription factor is an
important regulator of cardiac muscle cells. The present study
demonstrates that anthracyclines can down-regulate GATA-4 activity.
Treatment of HL-1 cardiac muscle cells or isolated adult rat
ventricular myocytes with anthracyclines such as daunorubicin and
doxorubicin decreased the level of GATA-4 DNA-binding activity. The
mechanism of decreased GATA-4 activity acts at the level of the GATA-4
gene, because anthracyclines caused significantly decreased levels of
GATA-4 protein and mRNA. The rate of decline in GATA-4 transcript
levels in the presence of actinomycin D was unaltered by
anthracyclines, indicating that these agents may affect directly GATA-4
gene transcription. To determine whether decreased GATA-4 levels are
functionally related to cardiac muscle cell death that can be induced
by anthracyclines, the ability of ectopic GATA factors to rescue
anthracycline-induced apoptosis was tested. Adenovirus-mediated
expression of either GATA-4 or GATA-6 was sufficient to attenuate the
incidence of apoptosis. Furthermore, suppression of GATA-4 DNA-binding
activity by a dominant negative mutant of GATA-4 induced the apoptosis.
These results suggest that the mechanism of anthracycline-induced
cardiotoxicity may involve the down-regulation of GATA-4 and the
induction of apoptosis.
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