Circulation, Vol 89, 799-809, Copyright © 1994 by American Heart Association
TJ Donohue, LD Dworkin, MN Lango, K Fliegner, RP Lango, JA Benstein, WR Slater and VM Catanese
BACKGROUND: Left ventricular hypertrophy is a generalized adaptation to
increased afterload, but the growth factors mediating this response have
not been identified. To explore whether the hypertrophic response was
associated with changes in local insulin-like growth factor-I (IGF- I) gene
regulation, we examined the induction of the cardiac IGF-I gene in three
models of systolic hypertension and resultant hypertrophy. METHODS AND
RESULTS: The model systems were suprarenal aortic constriction,
uninephrectomized spontaneously hypertensive rats (SHR), and
uninephrectomized, deoxycorticosterone-treated, saline-fed rats (DOCA
salt). Systolic blood pressure reached hypertensive levels at 3 to 4 weeks
in all three systems. A differential increase in ventricular weight to body
weight (hypertrophy) occurred at 3 weeks in the SHR and aortic constriction
models and at 4 weeks in the DOCA salt model. Ventricular IGF-I mRNA was
detected by solution hybridization/RNase protection assay. IGF-I mRNA
levels increased in all three systems coincident with the onset of
hypertension and the development of ventricular hypertrophy. Maximum
induction was 10-fold over control at 5 weeks in the aortic constriction
model, 8-fold at 3 weeks in the SHR, and 6-fold at 6 weeks in the DOCA salt
model. IGF-I mRNA levels returned to control values by the end of the
experimental period despite continued hypertension and hypertrophy in all
three systems. In contrast, ventricular c-myc mRNA content increased
twofold to threefold at 1 week and returned to control levels by 2 weeks.
Ventricular IGF-I receptor mRNA levels were unchanged over the time course
studied. The increased ventricular IGF-I mRNA content was reflected in an
increased ventricular IGF-I protein content, as determined both by
radioimmunoassay and immunofluorescence histochemistry. CONCLUSIONS: We
conclude that (1) hypertension induces significant increases in cardiac
IGF-I mRNA and protein that occur coordinately with its onset and early in
the development of hypertrophy, (2) IGF-I mRNA levels normalize as the
hypertrophic response is established, (3) in comparison to IGF-I, both
c-myc and IGF-I receptor genes are differentially controlled in
experimental hypertension. These findings suggest that IGF-I may
participate in initiating ventricular hypertrophy in response to altered
loading conditions. The consistency of these findings in models of high-,
moderate-, and low-renin hypertension suggests that they occur
independently of the systemic renin-angiotensin endocrine axis.
ARTICLES
Induction of myocardial insulin-like growth factor-I gene expression in left ventricular hypertrophy
Department of Medicine, New York University Medical Center, NY 10016.
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