doi: 10.1161/01.RES.0000253139.82251.31
© 2006 American Heart Association, Inc.
Editorials |
ß-Catenin Nuclear Activation
Common Pathway Between Wnt and Growth Factor Signaling in Vascular Smooth Muscle Cell Proliferation?
From the Institut National de la Santé et de la Recherche Médicale (T.C., P.D., C.D.), Inserm U441, Pessac, France; Université Victor Segalen Bordeaux 2 (T.C., P.D., C.D.), Bordeaux, France; Department of Cardiology (T.C.), CHU Groupe Sud, Hôpital Haut Lévêque, Pessac, France.
Correspondence to Thierry Couffinhal, MD, PhD, Inserm U 441, Avenue du Haut-Lévêque, 33600 Pessac, France. E-mail thierry.couffinhal@bordeaux.inserm.fr
See related article, pages 1329–1337
Key Words: vascular cells • proliferation • ß-catenin • Wnt pathway
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Understanding how smooth muscle cells transition from a steady state to a proliferative state will have an important impact on our understanding of vascular pathology. In the present issue of Circulation Research, Quasnichka et al take an indepth look at the role of the ß-catenin/T-cell factor (TCF) signaling pathway in vascular smooth muscle cell (VSMC) proliferation.1 Although ß-catenin is the central component in the Wnt canonical pathway, and is regarded as a hallmark of Wnt pathway activation, the present article and other recent reports elucidate new insights into activation of the ß-catenin pathway and indicates, that ß-catenin activation appears to be intricately orchestrated by both Wnt and growth factor networks.
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Central Role and Sharp Regulation of ß-Catenin at the Molecular and Cellular Levels |
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At the plasma membrane, it controls cell-cell adhesion through its binding with cadherin in adherence junctions and also mediates the link between cadherin and the actin cytoskeleton through the molecular switch
-catenin.2,3 In addition, ß-catenin acts as a transcriptional activator and regulates transcription of target genes responsible for cell proliferation and differentiation.4 Literature diverges on the interpretation of the interplay between these pathways. It is still unclear if these 2 processes act in concert or independently.5,6
The Wnt system is 1 of the well-known potent pathways, which activates nuclear ß-catenin. In the absence of Wnt signal, free cytoplasmic ß-catenin is phosphorylated by serine/threonine kinases, casein Kinase I (CKI) and GSK3ß in a large APC/axin scaffolding complex that targets ß-catenin for degradation. In the presence of Wnt signaling, this destruction complex is disrupted, and dissociation of GSK3ß prevents phosphorylation
Related Article:
Circ. Res. 2006 99: 1329-1337.
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