Skip Navigation

Cardiovascular Research 2002 54(3):499-502; doi:10.1016/S0008-6363(02)00395-4
© 2002 by European Society of Cardiology
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 Doevendans, P. A.
Right arrow Articles by van Eys, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Doevendans, P. A.
Right arrow Articles by van Eys, G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

Smooth muscle cells on the move: the battle for actin

Pieter A. Doevendansa,b,* and Guillaume van Eysa,c

aDepartment of Cardiology, Cardiovascular Research Institute, Academic Hospital Maastricht, 6202 AZ Maastricht, The Netherlands
bInteruniversity Cardiology Institute of the Netherlands, PO Box 5800, 6202 AZ Maastricht, The Netherlands
cDepartment of Molecular Genetics, University of Maastricht, Maastricht, The Netherlands

* Corresponding author. Tel.: +31-43-387-5095; fax: +31-43-387-7081 p.doevendans@cardio.azm.nl

Received 11 March 2002; accepted 13 March 2002

The first 150 words of the full text of this article appear below.

See article by Blindt et al. [2] (pages 630–639) in this issue.


   1 Introduction
 
Restenosis has been troubling patients and cardiologists, following percutaneous transluminal coronary angioplasty (PTCA), since the technique was introduced [1]. Dedifferentiation, migration and proliferation of smooth muscle cell (SMC) can cause a new obstructive lesion, at the site of the mechanical intravascular balloon intervention. Gradually our knowledge about SMC mobility is increasing. This mobility is the consequence of SMC (de)differentiation. The ability of these cells to switch from a contractile to a synthetic/proliferative phenotype has been a prime target of research in the cardiovascular field. Although the different phenotypes of SMC have been known for years, the underlying signalling, changes in gene expression and protein activation and the mechanism of cell mobility adaptation, still remain to be resolved. Also the keys to the maintenance of SMC (de)differentiation are currently unknown. Many clues indicate a crucial role for actin . . . [Full Text of this Article]


   2 Moesin expression and function
 

   3 SMC signalling
 

   4 The battle for actin
 

   5 Differentiated vs. undifferentiated SMC
 

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
 J AndrolHome page
E. Antonioli, A. B. Cardoso, and H. F. Carvalho
Effects of Long-Term Castration on the Smooth Muscle Cell Phenotype of the Rat Ventral Prostate
J Androl, September 1, 2007; 28(5): 777 - 783.
[Abstract] [Full Text] [PDF]

Home page
 J AndrolHome page
E. Antonioli, H. H. M. Della-Colleta, and H. F. Carvalho
Smooth Muscle Cell Behavior in the Ventral Prostate of Castrated Rats
J Androl, January 1, 2004; 25(1): 50 - 56.
[Abstract] [Full Text] [PDF]