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(Circulation Research. 2000;87:532.)
© 2000 American Heart Association, Inc.

Editorial

Novel Genes for Mitogen-Independent Smooth Muscle Replication

Mark W. Majesky

From the Departments of Pathology and Cellular & Molecular Biology, Baylor College of Medicine, Houston, Tex.

Correspondence to Mark W. Majesky, PhD, Center for Cardiovascular Development, Department of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. E-mail mmajesky@bcm.tmc.edu

Key Words: embryo • autonomous growth • neointima • proliferation

	Introduction

 
Vascular smooth muscle cells (SMCs) are generally assumed to require mitogenic stimulation to replicate. The mitogen may originate in the circulation, be derived from nearby cell types in the vessel wall, or be produced by SMCs themselves. Regardless of the source of the mitogen, requirements for activation of cell surface growth factor receptors and consequent downstream signaling pathways have been guiding principles to understand SMC growth control in vivo. This long-held assumption is being challenged by Weiser-Evans et al¹ in this issue of Circulation Research. These authors report the cloning of novel genes expressed by SMCs that exhibit a mitogen-independent or autonomous growth phenotype in vitro. One of these cDNAs, emb8:embryonic growth–associated protein (emb8:EGAP), may be at least partially responsible for controlling autonomous growth potential in SMCs. The authors suggest that these newly identified emb genes may represent an entirely novel class of genes that confer autonomous growth potential to SMCs during high rates of replication in vivo (during development, wound repair, and intimal disease).

	Autonomous Growth Phenotype

 
The concept of a self-driven, autonomous growth phenotype for vascular SMCs stems, in part, from work begun by Cook et al² about 10 years ago. Their initial goal was to define factors produced during normal vascular development that function to shut off SMC replication in the late fetal and early postnatal periods. The assumption was that SMCs produce a growth-inhibitory pericellular matrix and that a better understanding of the composition of this natural growth inhibitory matrix and how it was produced would lead to more . . . [Full Text of this Article]

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