Expression of coxsackievirus and adenovirus receptor in neointima of the rat carotid artery

被引:11
作者
Nasuno, A
Toba, K
Ozawa, T
Hanawa, H
Osman, Y
Hotta, Y
Yoshida, K
Saigawa, T
Kato, K
Kuwano, R
Watanabe, K
Aizawa, Y
机构
[1] Niigata Univ, Grad Sch Med & Dent Sci, Div Cardiol, Niigata 9518510, Japan
[2] Niigata Univ, Grad Sch Med & Dent Sci, Div Hematol, Niigata 9518510, Japan
[3] Niigata Univ, Grad Sch Med & Dent Sci, Mol Genet Res Lab, Niigata 9518510, Japan
[4] Niigata Coll Pharm, Dept Clin Pharmacol, Niigata 95021, Japan
关键词
coxsackievirus and adenovirus receptor; CAR; intimal hyperplasia; vascular smooth muscle cells; balloon injury;
D O I
10.1016/s1054-8807(03)00137-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Our previous study revealed that the coxsackievirus and adenovirus receptor (CAR) is a homophilic cell adhesion molecule and may function as a sensor of cell-cell interactions in the brain and damaged heart. In this study, we investigated if CAR expression is involved in the formation of neointimal hyperplasia using a balloon injury model of rat carotid artery. Cultured vascular smooth muscle cells (SMCs) from rat aorta were also studied. CAR antigen was constitutively detected in the endothelial cells (ECs) but not in SMCs before injury. On Day 5 after balloon injury, CAR was expressed strongly in the first layer of medial SMCs. Neointimal hyperplasia was observed on Day 7, and strong expressions of CAR concomitantly with proliferating cell nuclear antigen (PCNA) were obvious in the neointimal SMCs, while CAR in medial SMCs disappeared. The expression of CAR mRNA reached a peak on Day 7 and declined gradually to the basal levels. When the ECs regenerated on Day 14, CAR antigen was observed in the ECs but disappeared in the neointima. CAR together with PCNA was expressed abundantly in the proliferating SMCs in vitro and diminished in cells grown to a confluent state. The abundant expression of CAR in the neointima may facilitate an adenoviral gene therapy. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:79 / 84
页数:6
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