Skip Navigation

Cardiovascular Research 2006 71(1):170-178; doi:10.1016/j.cardiores.2006.03.003
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
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
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Zargham, R.
Right arrow Articles by Thibault, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zargham, R.
Right arrow Articles by Thibault, G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

{alpha}8 Integrin expression is required for maintenance of the smooth muscle cell differentiated phenotype

Ramin Zargham and Gaétan Thibault*

Institut de recherches cliniques de Montréal, Université de Montréal and Department of Experimental Medicine, McGill University, 110, avenue des Pins ouest, Montréal, Québec, Canada H2W 1R7

* Corresponding author. Tel.: +1 514 987 5613; fax: +1 514 987 5585. Email address: thibaug{at}ircm.qc.ca

Objective Vascular smooth muscle cell (VSMC) de-differentiation is a prerequisite for migration from the tunica media to the intima after vascular injury. Integrin cell adhesion molecules participate in VSMC phenotype modulation. {alpha}8β1 Integrin is a differentiation marker of VSMCs and its knockdown heightens migration. In the present study, we examined whether or not {alpha}8 integrin is required for the maintenance of VSMC differentiated phenotype.

Methods {alpha}8 Integrin in rat VSMC was knocked down by short interference RNA (siRNA) targeting {alpha}8 integrin in comparison to a non-silencing siRNA. Cytoskeletal and morphological changes in VSMC were examined by immunofluorescence staining. The expression of phenotype-dependent markers was analyzed by immunoblotting.

Results {alpha}8 Integrin gene silencing evoked drastic changes in characteristics of the VSMC differentiated phenotype, including VSMC morphology, actin fibre organization, focal adhesion assembly and the expression of phenotype-dependent markers in favor of de-differentiation. Then, we investigated whether or not phenotype modulation induced by {alpha}8 integrin gene silencing could be reversed by an inducer of VSMC differentiation. Transforming growth factor-β (TGF-β) failed to upregulate smooth muscle-myosin heavy chain as well as the assembly of parallel actin fibres in VSMCs transfected by siRNA-{alpha}8. In addition, TGF-β-induced vinculin localization at the tip of the cells was impaired by {alpha}8 integrin gene silencing.

Conclusion These data suggest that {alpha}8 integrin expression is required for maintenance of the VSMC differentiated phenotype, a state that is crucial for non-motile VSMCs.

KEYWORDS Angioplasty; Atherosclerosis; Cell differentiation; Cytoskeleton and smooth muscle


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


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
Y. Wu, Y. Huang, B. P. Herring, and S. J. Gunst
Integrin-linked kinase regulates smooth muscle differentiation marker gene expression in airway tissue
Am J Physiol Lung Cell Mol Physiol, December 1, 2008; 295(6): L988 - L997.
[Abstract] [Full Text] [PDF]


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.