Hypertension, Vol 13, 706-711, Copyright © 1989 by American Heart Association
AJ Naftilan, RE Pratt, CS Eldridge, HL Lin and VJ Dzau
Angiotensin II (Ang II) has been shown to cause hypertrophy of cultured
quiescent rat aortic smooth muscle cells. This observation along with the
recent demonstration of angiotensinogen messenger RNA (mRNA) in the vessel
wall has led us to postulate a role for Ang II in hypertensive smooth
muscle hypertrophy. One of the earliest responses in a wide variety of
cells in response to a growth-promoting agent is the induction of the
proto-oncogene c-fos. To investigate the mechanism of the action of Ang II,
we investigated the effect of Ang II on the expression of the c-fos gene in
rat aortic smooth muscle cells that were made quiescent by being grown in a
defined serum-free media for 48 hours. Ang II (10(-6)-10(-10) M) resulted
in a dose-dependent increase in c-fos mRNA expression. This induction was
angiotensin-receptor specific since it was completely abolished by the
competitive inhibitor saralasin. Inhibition of protein synthesis did not
block the rise in c- fos mRNA expression; it resulted in a superinduction
and stabilization of the c-fos mRNA. Using a nuclear runoff transcription
assay, we demonstrated that Ang II stimulated the transcription rate of the
c-fos gene. This activation of c-fos gene expression may be an important
mechanism in the angiotensin-induced smooth muscle hypertrophy.
ARTICLES
Angiotensin II induces c-fos expression in smooth muscle via transcriptional control
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
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