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Cardiovascular Research Advance Access first published online on July 25, 2009
This version [Corrected Proof] published online on August 13, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp263
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

Trichostatin A enhances proliferation and migration of vascular smooth muscle cells by downregulating thioredoxin 1

Seungjeong Song1, Sang Won Kang2 and Chulhee Choi1,*

1 Cell signaling and Bioimaging Laboratory, Department of Bio and Brain Engineering, KAIST, 335 Gwahangno, Yuseong-gu, Daejeon 305-701, Korea
2 Department of Life Science and Center for Cell Signaling and Drug Discovery Research, Ewha Womans University, Seoul 127-750, Korea

* Corresponding author. Tel: +82 42 350 4321, Fax: +82 42 350 4380, Email: cchoi{at}kaist.ac.kr

Aims: A reduction in the level of thioredoxin 1 (Trx1) has been proposed as a possible mechanism for the tumor-specific growth arrest caused by inhibition of histone deacetylases (HDACs). In this study, we investigated the effect of trichostatin A (TSA), a potent HDAC inhibitor, on the proliferation and migration of vascular smooth muscle cells (VSMCs), and we examined the role of reduced Trx1 levels in this effect.

Methods and results: TSA treatment time-dependently decreased Trx1 expression in rat VSMCs at both the mRNA and protein levels. It also enhanced platelet-derived growth factor (PDGF)-induced proliferation and migration of the VSMCs. By potentiating Akt phosphorylation, the siRNA-induced downregulation of Trx1 also enhanced VSMC proliferation and migration in response to PDGF or serum treatment. Consistent with these results, TSA administration increased neointimal thickening in a murine model of post-angioplastic restenosis.

Conclusion: These data demonstrate that TSA enhances vascular proliferative activity by downregulating Trx1, thus activating an Akt-dependent pathway. Our results indicate that, in addition to its apoptotic effects in tumour cells, the downregulation of Trx1 has a proliferative role in primary VSMCs.

KEYWORDS Histone deacetylases; Thioredoxin; Vascular smooth muscle cells; Proliferation; Migration

Time for primary reveiw: 16 days


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