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

Seungjeong Song, Sang Won Kang, Chulhee Choi

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


AimsA 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 resultsTSA 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.ConclusionThese 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.

Original languageEnglish
Pages (from-to)241-249
Number of pages9
JournalCardiovascular Research
Issue number1
StatePublished - Jan 2010

Bibliographical note

Funding Information:
This research was supported by a grant from the Korea Health 21 R&D Project (A060687) of the Ministry of Health and Welfare, Republic of Korea (to C.C.) and 21C Frontier Functional Proteomics Project (FPR08-B1-190) of Ministry of Education, Science & Technology (to S.W.K.). Funding to pay the Open Access publication charges for this article was provided by Chung Moon Soul Center for Bio-Information and Electronics.


  • Histone deacetylases
  • Migration
  • Proliferation
  • Thioredoxin
  • Vascular smooth muscle cells


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