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Published 8 May 2006. doi:10.1083/jcb.200508121
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 3, 417-429
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Article

The Fat1 cadherin integrates vascular smooth muscle cell growth and migration signals



Rong Hou, Liming Liu, Syed Anees, Shungo Hiroyasu, and Nicholas E.S. Sibinga

Departments of Medicine (Cardiovascular Division) and of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461

Correspondence to Nicholas Sibinga: nsibinga{at}aecom.yu.edu

The significance of cadherin superfamily proteins in vascular smooth muscle cell (VSMC) biology is undefined. Here we describe recent studies of the Fat1 protocadherin. Fat1 expression in VSMCs increases significantly after arterial injury or growth factor stimulation. Fat1 knockdown decreases VSMC migration in vitro, but surprisingly, enhances cyclin D1 expression and proliferation. Despite limited similarity to classical cadherins, the Fat1 intracellular domain (Fat1IC) interacts with ß-catenin, inhibiting both its nuclear localization and transcriptional activity. Fat1 undergoes cleavage and Fat1IC species localize to the nucleus; however, inhibition of the cyclin D1 promoter by truncated Fat1IC proteins corresponds to their presence outside the nucleus, which argues against repression of ß-catenin–dependent transcription by nuclear Fat1IC. These findings extend recent observations about Fat1 and migration in other cell types, and demonstrate for the first time its anti-proliferative activity and interaction with ß-catenin. Because it is induced after arterial injury, Fat1 may control VSMC functions central to vascular remodeling by facilitating migration and limiting proliferation.

Abbreviations used in this paper: Ftl, Fat-like; IC, intracellular; MASMC, mouse aortic smooth muscle cell; qPCR, quantitative PCR; RASMC, rat aortic smooth muscle cell; siRNA, small interfering RNA; VSMC, vascular smooth muscle cell.


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