Skip Navigation

Cardiovascular Research 2006 72(1):60-68; doi:10.1016/j.cardiores.2006.06.022
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 Mahadevan, V. S.
Right arrow Articles by Bayraktutan, U.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mahadevan, V. S.
Right arrow Articles by Bayraktutan, U.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2006, European Society of Cardiology

Internal mammary artery smooth muscle cells resist migration and possess high antioxidant capacity

Vaikom S. Mahadevana,1, Malcolm Campbella,1, Pascal P. McKeowna and Ulvi Bayraktutana,b,*

aDivision of Medicine and Therapeutics, Institute of Clinical Science, Queen's University Belfast, UK
bDivision of Stroke Medicine, Clinical Sciences Building, University of Nottingham, Hucknall Road, Nottingham NG5 1PB, England, UK

* Corresponding author. Division of Stroke Medicine, Clinical Sciences Building, University of Nottingham, Hucknall Road, Nottingham NG5 1PB, England, UK. Tel.: +44 115 8231764; fax: +44 115 8231767. Email address: ulvi.bayraktutan{at}nottingham.ac.uk

Objective: This study investigated whether differences exist in atherogen-induced migratory behaviors and basal antioxidant enzyme capacity of vascular smooth muscle cells (VSMC) from human coronary (CA) and internal mammary (IMA) arteries.

Methods: Migration experiments were performed using the Dunn chemotaxis chamber. The prooxidant [NAD(P)H oxidase] and antioxidant [NOS, superoxide dismutase, catalase and glutathione peroxidase] enzyme activities were determined by specific assays.

Results: Chemotaxis experiments revealed that while both sets of VSMC migrated towards platelet-derived growth factor-BB (1–50 ng/ml) and angiotensin II (1–50 nM), neither oxidized-LDL (ox-LDL, 25–100 µg/ml) nor native LDL (100 µg/ml) affected chemotaxis in IMA VSMC. However, high dose ox-LDL produced significant chemotaxis in CA VSMC that was inhibited by pravastatin (100 nM), mevastatin (10 nM), losartan (10 nM), enalapril (1 µM), and MnTBAP (a free radical scavenger, 50 µM). Microinjection experiments with isoprenoids i.e. geranylgeranylpyrophosphate (GGPP) and farnesylpyrophosphate (FPP) showed distinct involvement of small GTPases in atherogen-induced VSMC migration. Significant increases in antioxidant enzyme activities and nitrite production along with marked decreases in NAD(P)H oxidase activity and O2Formula levels were determined in IMA versus CA VSMC.

Conclusions: Enhanced intrinsic antioxidant capacity may confer on IMA VSMC resistance to migration against atherogenic agents. Drugs that regulate ox-LDL or angiotensin II levels also exert antimigratory effects.

KEYWORDS Atherosclerosis; Arteries; Oxygen radicals; Nitric oxide


1 Contributed equally to the manuscript.

Available online 27 June 2006 Time for primary review 32 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.