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(Circulation Research. 2004;94:706.)
© 2004 American Heart Association, Inc.

Editorials

Beyond the Endothelium

NF-B Regulation of Smooth Muscle Function

Elaine W. Raines, Kyle J. Garton, Nicola Ferri

From the Department of Pathology, University of Washington School of Medicine, Seattle, Wash. Present address for N.F. is Department of Pharmacological Sciences, University of Milan, Milan, Italy.

Correspondence to Elaine W. Raines, Department of Pathology, Harborview Medical Center, 325 9th Ave, Box 359675, Seattle, WA 98104-2499. E-mail ewraines@u.washington.edu

Key Words: restenosis • inflammation • cell adhesion molecules • smooth muscle cells • chemokines

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

Vascular smooth muscle cells (SMCs) are important for structural integrity of the medial wall but are also central to vascular remodeling in response to injury. Although highly differentiated cells with the ability to regulate vascular tone and extracellular matrix synthesis, SMCs are also very plastic cells that can rapidly respond to local injury and dramatically modify their phenotype. A transcriptional factor implicated in vascular disease is nuclear factor-B (NF-B), a pleiotropic protein complex activated by proinflammatory signals and cellular stress that has been shown to regulate over a hundred cellular genes and different transcriptional programs (Figure). An intensive effort over the past 10 years has focused on the potential role of NF-B in the regulation of endothelial and inflammatory cell responses in vascular pathologies.¹ However, recent in vitro and in vivo evidence highlights the importance of NF-B in regulating SMC gene expression and cellular functions after injury.

View larger version (34K): [in this window] [in a new window]   NF-B activates key transcriptional programs in smooth muscle cells. NF-B activation in vascular pathology is schematically presented. After vascular injury, a number of different initiation factors lead to activation of the IB kinase (IKK) complex that specifically phosphorylates IB, which then undergoes rapid degradation by the proteosome. After release from the inhibitor, NF-B dimers translocate from the cytoplasm to the nucleus where they initiate transcriptional programs. Overexpression of IB in vitro and in vivo blocks NF-B activation and has allowed definition of key transcriptional pathways in the SMC response to . . . [Full Text of this Article]

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