Skip Navigation

Cardiovascular Research 2007 74(1):169-179; doi:10.1016/j.cardiores.2007.01.017
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Liu, X.-m.
Right arrow Articles by Durante, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, X.-m.
Right arrow Articles by Durante, W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2007, European Society of Cardiology

Butylated hydroxyanisole stimulates heme oxygenase-1 gene expression and inhibits neointima formation in rat arteries

Xiao-ming Liua,b, Mohammed A. Azama,b, Kelly J. Peytona,b, Diana Ensenatb, Amit N. Keswanib, Hong Wangc and William Durantea,b,*

aDepartment of Medical Pharmacology and Physiology, University of Missouri, M409 Medical Sciences Building, One Hospital Drive, Columbia, MO 65212, United States
bDepartment of Medicine, Baylor College of Medicine, Houston, TX 77030, United States
cDepartment of Pharmacology, Temple University, Philadelphia, PA 191140, United States

* Corresponding author. Department of Medical Pharmacology and Physiology, University of Missouri, M409 Medical Sciences Building, One Hospital Drive, Columbia, MO 65212, United States. Tel.: +1 573 882 3886; fax: +1 573 884 4276. Email address: durantew{at}health.missouri.edu

Objective: Butylated hydroxyanisole (BHA) is a synthetic phenolic compound that is a potent inducer of phase II genes. Since heme oxygenase-1 (HO-1) is a vasoprotective protein that is upregulated by phase II inducers, the present study examined the effects of BHA on HO-1 gene expression and vascular smooth muscle cell proliferation.

Methods: The regulation of HO-1 gene expression and vascular cell growth by BHA was studied in cultured rat aortic smooth muscle cells and in balloon injured rat carotid arteries.

Results: Treatment of cultured smooth muscle cells with BHA stimulated the expression of HO-1 protein, mRNA and promoter activity in a time- and concentration-dependent manner. BHA-mediated HO-1 expression was dependent on the activation of NF-E2-related factor-2 by p38 mitogen-activated protein kinase. BHA also inhibited cell cycle progression and DNA synthesis in an HO-1-dependent manner. In addition, the local perivascular delivery of BHA immediately after arterial injury of rat carotid arteries induced HO-1 protein expression and markedly attenuated neointima formation.

Conclusions: These studies demonstrate that BHA stimulates HO-1 gene expression in vascular smooth muscle cells, and that the induction of HO-1 contributes to the antiproliferative actions of this phenolic antioxidant. BHA represents a potentially novel therapeutic agent in treating or preventing vasculoproliferative disease.

KEYWORDS Smooth muscle; Arteries; Gene expression; Restenosis; Angioplasty

Time for primary review 21 days


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.