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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1701.)
© 2000 American Heart Association, Inc.

Editorials

AIF-1 in the Activated Smooth Muscle Cell

Spectator or Participant?

Francis J. Miller, Jr

From the Department of Internal Medicine, University of Iowa, Iowa City.

Correspondence to Francis J. Miller, Jr, MD, Assistant Professor, Department of Internal Medicine, E314-4 GH, University of Iowa Hospitals, Iowa City, IA 52242. E-mail francis-miller@uiowa.edu (Arterioscler Thromb Vasc Biol. 2000;20:1701-1703.)

Key Words: Editorials • smooth muscle cell • blood vessel • vascular injury • cell signaling

In response to an environmental stimulus, a subset of smooth muscle cells (SMCs) within the vessel wall is induced to increase expression of multiple genes (SMC activation). Balloon injury, for example, initiates a cascade of repair mechanisms that result in migration and proliferation of SMCs, forming a neointima. SMC activation likely contributes to the vascular remodeling associated with hypertension, atherosclerosis, and restenosis after balloon angioplasty. Cytokines and growth factors are among the signals to activate induction of genes in otherwise-quiescent SMCs. Recent advances in vascular biology have identified the molecular signals that mediate these processes, the cytokine-responsive genes that characterize the activated SMCs, and the pathophysiological importance of their gene products.

One of the first genes expressed in response to vascular injury is the immediate-early gene (egr-1), which activates expression of multiple transcription factor genes. This cascade may be responsible for induction of the response to injury, including SMC proliferation.¹ The expression of a substantial number of genes has been proposed to differentiate intimal SMCs from medial SMCs.² In addition to activation of transcription and translation factors, there is increased expression of genes for receptors,^{3 4} growth factors,^{4 5 6} cytokines,^{5 7} adhesion molecules,⁸ extracellular matrix,^{9 10} and proapoptotic mediators¹¹ in the activated SMCs.

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Autieri and colleagues¹² report that SMC expression of allograft inflammatory factor-1 (AIF-1) is also increased in response to vascular injury. AIF-1 was first identified by Utans et al¹³ as a novel myeloid factor in rats, selectively expressed by inflammatory cells, and . . . [Full Text of this Article]

This article has been cited by other articles:

				M. V. Autieri and C. M. Carbone Overexpression of Allograft Inflammatory Factor-1 Promotes Proliferation of Vascular Smooth Muscle Cells by Cell Cycle Deregulation Arterioscler Thromb Vasc Biol, September 1, 2001; 21(9): 1421 - 1426. [Abstract] [Full Text] [PDF]