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(Circulation. 2003;108:1164.)
© 2003 American Heart Association, Inc.

Focused Perspective

Cyclic AMP Response Element-Binding Protein in the Vessel Wall

Good or Bad?

Jane E.B. Reusch, MD; Dwight J. Klemm, PhD

From the Denver VA Medical Center and University of Colorado Health Sciences Center.

Correspondence to Jane E.B. Reusch, MD, Denver VA Medical Center Endo 111-H, 1055 Clermont St, Denver, CO 80220. E-mail jane.reusch@uchsc.edu

Key Words: Editorials • protein, DNA-binding, cyclic AMP–responsive • atherosclerosis • restenosis • cells, smooth muscle, vascular

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Atherosclerosis and postangioplasty restenosis are leading causes of death in the Western world. Recent advances in our understanding of vascular biology would suggest that targeting specific signals in the post–balloon injury vessel or in persons prone to development of atherosclerosis could decrease lesion formation and in the long term decrease cardiovascular events. In light of this, numerous laboratories around the world are investigating the functional activities of the various cellular components of the atherosclerotic plaque, including vascular smooth muscle cells (SMCs), endothelial cells (ECs), and monocyte/macrophages.

See p 1246

One of the strategies for examining vascular wall response to injury in animal models has been the use of the balloon injury model. In this model, a balloon catheter is used to cause an injury and denuding of the endothelium. The animals are monitored serially over 7, 14, and 28 days for narrowing of the blood vessel lumen after injury. This model traditionally has been used to examine activation of SMCs and their proliferative response. In response to balloon injury, vascular SMCs (which are normally contractile and quiescent [nonproliferative]) are released into a proliferation phase by the injury and loss of the endothelium.

Immunostaining studies have suggested that the majority of the cells that cause luminal narrowing are SMCs.¹ However, recent studies have also demonstrated the presence of inflammatory cells in this model.² Macrophages are observed both in the balloon injury model and in balloon injury/stent models. Thus, interfering with either SMC function or macrophage activation would be expected to have . . . [Full Text of this Article]

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Apoptosis Induced by Inhibition of Cyclic AMP Response Element–Binding Protein in Vascular Smooth Muscle Cells

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Circulation 2003 108: 1246-1252. [Abstract] [Full Text]

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