(Circulation. 1997;95:1515-1522.)
© 1997 American Heart Association, Inc.
Articles |
Inhibition of Intimal Hyperplasia After Balloon Injury by Antibodies to Intercellular Adhesion Molecule-1 and Lymphocyte Function–Associated Antigen-1
From the Departments of Pathology II (H.Y., A.N., M.M.) and Internal Medicine III (T.I., H.M.), Kurume University School of Medicine, Kurume, Fukuoka 830, Japan.
Correspondence to Hideo Yasukawa, MD, Department of Pathology II, Kurume University School of Medicine, 67 Asahi-machi, Kurume, Fukuoka 830, Japan.
Background Although intercellular adhesion molecule-1 (ICAM-1) is known to be expressed in balloon-injured arteries, it remains unknown whether ICAM-1 plays a role in the progression of intimal hyperplasia (IH) induced by balloon injury.
Methods and Results We examined the ICAM-1 expression in rat carotid arteries at 1, 2, 5, 7, 10, and 14 days after injury by immunohistochemistry. Medial smooth muscle cells (SMC) expressed ICAM-1 intensely at 1 to 2 days after injury. The regenerating endothelial cells expressed ICAM-1 more than did those of intact carotid arteries. To investigate the effects of monoclonal antibodies (MAbs) on IH, we examined the intima/medial ratio of arteries at 2 weeks after injury in five treatment groups: nonimmune IgG, anti-membrane glycoprotein MAb, anti–lymphocyte function–associated antigen-1 (LFA-1) MAb, anti–ICAM-1 MAb, and anti–ICAM/LFA-1 MAb. Treatments were administered intravenously into rats for 6 consecutive days after injury. MAb against LFA-1 alone or membrane glycoprotein had no effect on IH. The intima/media ratios in anti–ICAM-1 MAb–treated and anti–ICAM-1/LFA-1 MAb–treated animals were significantly less than those in nonimmune IgG–treated and anti–membrane glycoprotein MAb–treated animals (P<.05).
Conclusions Balloon injury induced or upregulated the ICAM-1 expression on vascular SMC and on regenerating endothelial cells. MAb against ICAM-1 or ICAM-1/LFA-1 attenuated IH. These results suggest that ICAM-1 may play a role in the progression of IH after injury in rats.
Key Words: atherosclerosis • muscle, smooth • stenosis • angioplasty • remodeling
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