Copyright © 2005, European Society of Cardiology
Oxidized LDL receptor LOX-1 is involved in neointimal hyperplasia after balloon arterial injury in a rat model
aDepartment of Vascular Physiology, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan
bDepartment of Molecular Pathophysiology, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka 565-0871, Japan
cDepartment of Pathology, Osaka City University Medical School, Osaka 545-8585, Japan
dDepartment of Cardiology, Osaka City General Hospital, Osaka 534-0021, Japan
eDivision of Cardiovascular Medicine, University of Arkansas Medical School, Little Rock, AR, United States
*Corresponding author. Department of Vascular Physiology, National Cardiovascular Center research Institute, 5-7-1, Fujishirodai, Suita, Osaka, 565-8565, Japan. Tel.: +81 6 6833 5012x2518; fax: +81 6 6835 5329. Email address: t-sawamura{at}umin.ac.jp
Objective: LOX-1 is a multi-ligand receptor originally identified as the endothelial oxidized LDL receptor. LOX-1 expression is also induced in smooth muscle cells in response to proinflammatory and oxidative stimuli. Here, we report on the role of LOX-1 in intimal hyperplasia, in which proinflammatory and oxidative stimuli are increased.
Methods and results: Left common carotid artery of rat was injured by a balloon catheter. The expression of LOX-1 was significantly increased within 24 h after the balloon injury and peaked at day 7. LOX-1 expression was observed predominantly in medial smooth muscle cells until day 3, and then shifted to predominantly intimal smooth muscle cells. At day 14, the expression was concentrated in the regenerated endothelial cells. To examine the contributory role of LOX-1 in the growth of intimal smooth muscle cells, rats were administered anti-LOX1 antibody intravenously every 3 days after balloon injury. Anti-LOX-1 antibody administration effectively suppressed intimal hyperplasia, oxidative stress, and leukocyte infiltration compared with control IgG. These findings suggest the importance of LOX-1 expression in the pathogenesis of neointimal formation in conjunction with oxidative stress and leukocyte infiltration.
Conclusion: The LOX-1 expressed in smooth muscle cells is involved in intimal hyperplasia in a rat model of balloon injury. Manipulation of LOX-1 activity is a novel potential therapeutic target to prevent restenosis after angioplasty.
KEYWORDS Restenosis; Neointimal formation; LOX-1; Smooth muscle cells
Time for primary review 31 days
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