3,3′diindolylmethane suppresses vascular smooth muscle cell phenotypic modulation and inhibits neointima formation after carotid injury3、3u2032diindolylmethane抑制血管平滑肌细胞表型调制,抑制neointima颈动脉损伤后形成.pdfVIP

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3,3′diindolylmethane suppresses vascular smooth muscle cell phenotypic modulation and inhibits neointima formation after carotid injury3、3u2032diindolylmethane抑制血管平滑肌细胞表型调制,抑制neointima颈动脉损伤后形成.pdf

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3,3′diindolylmethane suppresses vascular smooth muscle cell phenotypic modulation and inhibits neointima formation after carotid injury3、3u2032diindolylmethane抑制血管平滑肌细胞表型调制,抑制neointima颈动脉损伤后形成

3,39Diindolylmethane Suppresses Vascular Smooth Muscle Cell Phenotypic Modulation and Inhibits Neointima Formation after Carotid Injury Hongjing Guan1,2, Lihua Zhu1,2, Mingyue Fu1,2, Da Yang1,2, Song Tian1,2, Yuanyuan Guo1,2, Changping Cui1,2, Lang Wang1,2, Hong Jiang1,2* 1 Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, People’s Republic of China, 2 Cardiovascular Research Institute of Wuhan University, Wuhan, People’s Republic of China Abstract Background: 3, 39diindolylmethane (DIM), a natural phytochemical, has shown inhibitory effects on the growth and migration of a variety of cancer cells; however, whether DIM has similar effects on vascular smooth muscle cells (VSMCs) remains unknown. The purpose of this study was to assess the effects of DIM on the proliferation and migration of cultured VSMCs and neointima formation in a carotid injury model, as well as the related cell signaling mechanisms. Methodology/Principal Findings: DIM dose-dependently inhibited the platelet-derived growth factor (PDGF)-BB-induced proliferation of VSMCs without cell cytotoxicity. This inhibition was caused by a G0/G1 phase cell cycle arrest demonstrated by fluorescence-activated cell-sorting analysis. We also showed that DIM-induced growth inhibition was associated with the inhibition of the expression of cyclin D1 and cyclin-dependent kinase (CDK) 4/6 as well as an increase in p27Kip1 levels in PDGF-stimulated VSMCs. Moreover, DIM was also found to modulate migration of VSMCs and smooth muscle-specific contractile marker expression. Mechanistically, DIM negatively modulated PDGF-BB-induced phosphorylation of PDGF- recptorb (PDGF-Rb) and the activities of downstream signaling molecules including Akt/glycogen synthase kinase(GSK)3b, extracellular signal-regulated kinase1/2 (ERK1/2), and signal transducers and activators