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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:2063.)
© 2004 American Heart Association, Inc.

Vascular Biology

E-Selectin Blockade Decreases Adventitial Inflammation and Attenuates Intimal Hyperplasia in Rat Carotid Arteries After Balloon Injury

Ryo Gotoh; Jun-ichi Suzuki; Hisanori Kosuge; Tsunekazu Kakuta; Shinji Sakamoto; Masayuki Yoshida; Mitsuaki Isobe

From the Department of Cardiovascular Medicine (R.G., J.S., H.K., T.K., M.I.), Tokyo Medical and Dental University, Tokyo, Japan; Pharmaceutical Frontier Research Laboratories (S.S.), JT Inc, Yokohama, Japan; and the Department of Medical Biochemistry (M.Y.), Tokyo Medical and Dental University, Tokyo, Japan.

Correspondence to Mitsuaki Isobe, MD, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. E-mail isobemi.cvm{at}tmd.ac.jp

Objective— Inflammation is one of the initial repair processes after vascular injury. E-selectin facilitates adherence of leukocytes to vascular endothelium at the site of inflammation. Because the role of E-selectin in this process is not fully understood, we studied the role of E-selectin in vascular injury with a flow chamber model and a rat model of carotid artery injury.

Methods and Results— We established a rat aortic endothelial cell (RAEC) culture system from the aortas of adult male rats. When rat myelomonocytes were suspended in a flow chamber, rolling and adhesion to lipopolysaccharide (LPS)-stimulated RAECs were observed. Cell rolling and adhesion were greatly reduced by addition of anti–E-selectin monoclonal antibody (mAb). We then induced balloon injury in the left carotid arteries of rats. E-selectin expression was enhanced in endothelial cells at adventitial small vessels 7 days after injury. Rats with balloon injury were injected intraperitoneally with anti–E-selectin mAb for 8 days. Inflammatory cell infiltration was reduced by anti–E-selectin mAb treatment at the adventitia at 7 days after injury. This reduction was associated with attenuation of intimal hyperplasia in the rats treated with the mAb.

Conclusions— These data suggest that E-selectin regulates adventitial inflammation through leukocyte adhesion and contributes to the process of intimal hyperplasia after balloon injury.

E-selectin facilitates adherence of leukocytes at the site of inflammation. We studied the action of E-selectin in vascular injury with a rat model of carotid artery injury. The results suggested that E-selectin regulates adventitial inflammation through leukocyte adhesion and contributes to the process of intimal hyperplasia after balloon injury.

Key Words: adhesion molecules • adventitial inflammation • angioplasty • rat aortic endothelial cell • restenosis

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