Copyright © 2006, European Society of Cardiology
Internal mammary artery smooth muscle cells resist migration and possess high antioxidant capacity
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 O2
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
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