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(Circulation. 1997;95:1355-1356.)
© 1997 American Heart Association, Inc.

A Role for Intercellular Adhesion Molecule-1 in Restenosis

Edward F. Plow, PhD; Stanley E. D'Souza, MD

the Joseph J. Jacobs Center for Thrombosis and Vascular Biology, The Cleveland Clinic Foundation, Cleveland, Ohio.

Correspondence to Dr Edward F. Plow, Joseph J. Jacobs Center for Thrombosis and Vascular Biology, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195.

Key Words: Editorials • cells • angioplasty • intercellular adhesion molecule-1

	Introduction

 
With more than 30% of patients requiring an additional intervention within 1 year after PTCA, restenosis continues to be a clinical complication of enormous importance.¹ Because the nature of the causative event, neointimal hyperplasia arising from vascular injury, and the timing of the initiating event, the time of PTCA, are well defined, it seems that restenosis should be a ready target for treatment and prevention. Nevertheless, restenosis has remained stubbornly resistant to therapy for almost 20 years. This contradiction implies that our knowledge of the molecular and cellular mechanisms underlying restenosis is inadequate and/or that the therapeutic targets selected thus far have not been optimal. In the present issue of Circulation, Yasukawa et al² examine the role of ICAM-1 in intimal hyperplasia. These investigators show that ICAM-1 is expressed early and intensely in rat carotid arteries after balloon injury and that an MAb to ICAM-1 significantly suppresses intimal hyperplasia in the rat model of restenosis. Thus, this article provides new insights into the basic changes that occur within developing restenotic lesions, implicates ICAM-1 in the mechanisms leading to intimal hyperplasia, and identifies a new candidate target to consider for the treatment of restenosis.

ICAM-1 is a highly glycosylated cell surface protein of 95 kD. It is expressed at variable levels on EC, SMC, fibroblasts, several tumor cell lines, and circulating leukocytes.³ On cultured EC and SMC, the levels of ICAM-1 are dramatically upregulated on treatment with inflammatory mediators, such as TNF-, interferon-, interleukin-1, and bacterial lipopolysaccharide.^{4 5} TNF- . . . [Full Text of this Article]

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