Skip Navigation



Cardiovascular Research Advance Access [Accepted Manuscript] published online on October 19, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm045
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
77/1/211    most recent
cvm045v3
cvm045v2
cvm045v1
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 Teresa, P.
Right arrow Articles by Lina, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Teresa, P.
Right arrow Articles by Lina, B.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

LDL impair migration of human coronary vascular smooth muscle cells and induce changes in the proteomic profile of myosin light chain

Padró Teresa1, Peña Esther1, García-Arguinzonis Maisa1, Llorente-Cortes Vicenta1 and Badimon Lina1,2,

1 Cardiovascular Research Center, CSIC-ICCC, Hospital Santa Creu i Sant Pau, Barcelona, Spain
2 Cardiovascular Research Chair "Catalana Occidente", UAB, Barcelona, Spain

Correspondence: Badimon L. Cardiovascular Research Center, CSIC-ICCC, Hospital de la Santa Creu i Sant Pau, Av. S. Antoni M. Claret, 167 08025 Barcelona, Spain Tel: ++34 93 556 58 80 Fax: ++34 93 556 55 59 eMail.: lbadimon{at}csic-iccc.org

Aim: High risk atheromatous plaques contain significant extra- and intracellular lipid deposits and very low smooth muscle cell numbers in the intima. However, the mechanisms inducing vessel wall remodelling and high risk plaque composition are unknown. LDL infiltrate the vessel wall and become retained and aggregated (agLDL) in the intima by binding to extracellular matrix proteoglycans. The cellular responses triggered by agLDL are not fully understood. This study was designed to investigate the effects of agLDL on vascular remodeling and repair, specifically studying human coronary vascular smooth muscle cell (VSMC) functions.

Methods and results: Using a wound repair VSMC model system, we have shown that agLDL significantly impair cell migration. Proteomic analysis revealed a differential phenotypic pattern of myosin light chain and lower levels of phosphorylated myosin regulatory light chain (MRLC) in agLDL-exposed VSMC. LDL also induced changes in the subcellular localization of phosphorylated MRLC, with dephosphorylation strongly evident on the front edge of agLDL-treated migrating cells. PMA, a strong inducer of MLC phosphorylation, significantly reduced the effects of agLDL in VSMC migration. Inhibition of MLC kinase with ML9 did not affect MRLC dephosphorylation already induced by agLDL.

Conclusions: Our results indicate that LDL impair human VSMC migration and wound repair after injury. agLDL, and to a lesser extent nLDL, induce dephosphorylation of MRLC and striking changes in the subcellular localization of phosphorylated MRLC, a cytoskeleton protein involved in VSMC migration kinetics.

Time for primary review: 12 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.