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Magnolol attenuates neointima formation by inducing cell cycle arrest via inhibition of ERK1/2 and NF-κB activation in vascular smooth muscle cells : Magnolol attenuates neointima formation by inducing cell cycle arrest via inhibition of ERK1/2 and NF-kappa B activation in vascular smooth muscle cells

Cited 43 time in Web of Science Cited 40 time in Scopus
Authors

Karki, Rajendra; Ho, Oak-Min; Kim, Dong-Wook

Issue Date
2013-03
Publisher
Elsevier BV
Citation
Biochimica et Biophysica Acta - General Subjects, Vol.1830 No.3, pp.2619-2628
Abstract
Background: Endovascular injury induces switching of contractile phenotype of vascular smooth muscle cells (VSMCs) to synthetic phenotype, thereby causing proliferation of VSMCs leading to intimal thickening. The purpose of this study was to assess the effect of magnolol on the proliferation of VSMCs in vitro and neointima formation in vivo, as well as the related cell signaling mechanisms. Methods: Tumor necrosis factor alpha (TNF-alpha) induced proliferation of VSMCs was assessed using colorimetric assay. Cell cycle progression and mRNA expression of cell cycle associated molecules were determined by flow cytometry and reverse transcription polymerase chain reaction (RT-PCR) respectively. The signaling molecules such as ERK1/2, JNK, P38 and NF-kappa B were determined by Western blot analysis. In addition, rat carotid artery balloon injury model was performed to assess the effect of magnolol on neointima formation in vivo. Results: Oral administration of magnolol significantly inhibited intimal area and intimal/medial ratio (I/M). Our in vitro assays revealed magnolol dose dependently induced cell cycle arrest at G0/G1. Also, magnolol inhibited mRNA and protein expression of cyclin D1, cyclin E. CDK4 and CDK2 in vitro and in vivo. The cell cycle arrest was associated with inhibition of ERK1/2 phosphorylation and NF-kappa B translocation. Conclusion: Magnolol suppressed proliferation of VSMCs in vitro and attenuated neointima formation in vivo by inducing cell cycle arrest at G0/G1 through modulation of cyclin D1, cyclin E, CDK4 and CDK2 expression. General significance: Thus, the results suggest that magnolol could be a potential therapeutic candidate for the prevention of restenosis and atherosclerosis. (C) 2012 Elsevier B.V. All rights reserved.
ISSN
0304-4165
URI
https://hdl.handle.net/10371/203072
DOI
https://doi.org/10.1016/j.bbagen.2012.12.015
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  • College of Natural Sciences
  • School of Biological Sciences
Research Area Cytokine Storm, Host Defense, Innate Immunity in Metabolic and Inflammatory Diseases

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