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Oxidative Medicine and Cellular Longevity
Volume 2014, Article ID 572430, 9 pages
http://dx.doi.org/10.1155/2014/572430
Research Article

Resveratrol Inhibits Phenotype Modulation by Platelet Derived Growth Factor-bb in Rat Aortic Smooth Muscle Cells

1Cellbiocontrol Laboratory, Department of Medical Engineering, Yonsei University College of Medicine, 134 Shinchon-Dong, Seodaemun-Gu, Seoul 120-752, Republic of Korea
2Brain Korea 21 PLUS Project for Medical Science, Yonsei University, 134 Shinchon-Dong, Seodaemun-Gu, Seoul 120-752, Republic of Korea

Received 8 November 2013; Revised 8 January 2014; Accepted 27 January 2014; Published 10 March 2014

Academic Editor: Constantinos Pantos

Copyright © 2014 Mi Hee Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Dedifferentiated vascular smooth muscle cells (VSMCs) are phenotypically modulated from the contractile state to the active synthetic state in the vessel wall. In this study, we investigated the effects of resveratrol on phenotype modulation by dedifferentiation and the intracellular signal transduction pathways of platelet derived growth factor-bb (PDGF-bb) in rat aortic vascular smooth muscle cells (RAOSMCs). Treatment of RAOSMCs with resveratrol showed dose-dependent inhibition of PDGF-bb-stimulated proliferation. Resveratrol treatment inhibited this phenotype change and disassembly of actin filaments and maintained the expression of contractile phenotype-related proteins such as calponin and smooth muscle actin-alpha in comparison with only PDGF-bb stimulated RAOSMC. Although PDGF stimulation elicited strong and detectable Akt and mTOR phosphorylations lasting for several hours, Akt activation was much weaker when PDGF was used with resveratrol. In contrast, resveratrol only slightly inhibited phosphorylations of 42/44 MAPK and p38 MAPK. In conclusion, RAOSMC dedifferentiation, phenotype, and proliferation rate were inhibited by resveratrol via interruption of the balance of Akt, 42/44MAPK, and p38MAPK pathway activation stimulated by PDGF-bb.