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- Title
Internal mammary artery smooth muscle cells resist migration and possess high antioxidant capacity
- Authors
Mahadevan, Vaikom S.; Campbell, Malcolm; McKeown, Pascal P.; Bayraktutan, Ulvi
- Abstract
Abstract: 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.
- Subjects
BLOOD vessels; SMOOTH muscle; CHEMOTAXIS; NITRIC oxide
- Publication
Cardiovascular Research, 2006, Vol 72, Issue 1, p60
- ISSN
0008-6363
- Publication type
Article
- DOI
10.1016/j.cardiores.2006.06.022