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Vol. 62, Issue 4, 772-777, October 2002
Department of Pharmacy, Center of Drug Research, University of
Munich, Munich, Germany (U.B.H., A.M.V., V.M.D.); and Department of
Medicine, Division of Cardiology, Emory University, Atlanta, Georgia
(D.S., K.K.G.)
Resveratrol (RV), a polyphenolic substance found in grape skin, is
proposed to account in part for the protective effect of red wine in
the cardiovascular system. Angiotensin II (Ang II)-induced hypertrophy
of vascular smooth muscle cells (VSMCs) is a pivotal step in the
development of cardiovascular disease. The aims of this study were to
test the hypothesis that RV may alter Ang II-mediated hypertrophic VSMC
growth and to identify the putative underlying signaling pathways. We
show that RV indeed potently inhibits Ang II-induced
[3H]leucine incorporation in a concentration-dependent
manner (50 µM RV, 71% inhibition). Western blot analysis reveals
that phosphorylation of Akt/protein kinase B (PKB) and to a lesser
extent the mitogen-activated protein kinase extracellular
signal-regulated kinase (ERK) 1/2, both essentially involved in Ang
II-mediated hypertrophy, is dose dependently reduced by RV. Consistent
with these results, we show that RV attenuates phosphorylation of the
p70 ribosomal protein S6 kinase (p70S6K), a kinase
downstream of the ERK 1/2 as well as the Akt pathway, that is
implicated in Ang II-induced protein synthesis. Upstream of Akt/PKB RV
seems to mediate its antihypertrophic effect by inhibiting
phosphorylation of the phosphatidylinositol 3-kinase (PI3K)
rather than by activating phosphatases. In summary, we demonstrate for
the first time that RV inhibits Ang II-induced VSMC hypertrophy,
possibly by interfering mainly with the PI3K/Akt and
p70S6K but also with the ERK 1/2 signaling pathway. Thus,
this study delivers important new insight in the molecular pathways
that may contribute to the proposed beneficial effects of RV in
cardiovascular disease.
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