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Arterioscler Thromb Vasc Biol. 2007 Jul;27(7):1535-41. Epub 2007 May 3.

Acyclic retinoid inhibits neointima formation through retinoic acid receptor beta-induced apoptosis.

Author information

1
Department of Cardiovascular Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.

Abstract

OBJECTIVES:

Acyclic retinoid (ACR) is a synthetic retinoid with a high safety profile that has been pursued with high expectations for therapeutic use in prevention (recurrence) and treatment of malignancies. With the objective of addressing the therapeutic potential in the cardiovasculature, namely neointima formation, effects of ACR on neointima formation and the involved mechanisms were investigated.

METHODS AND RESULTS:

ACR was administered to cuff-injured mice which showed inhibition of neointima formation. Investigation of involved mechanisms at the cellular and molecular levels showed that ACR induces apoptosis of neointimal cells and this to be mediated by selective induction of retinoic-acid receptor beta (RARbeta) which shows growth inhibitory and proapoptotic effects on smooth muscle cells.

CONCLUSION:

We show that ACR inhibits neointima formation by inducing RARbeta which in turn inhibits cell growth and induces apoptosis. The retinoid, ACR, may be potentially exploitable for treatment and prevention of neointima formation.

PMID:
17478760
DOI:
10.1161/ATVBAHA.106.134114
[Indexed for MEDLINE]

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