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(Circulation Research. 2008;102:1.)
© 2008 American Heart Association, Inc.

Editorials

Partners in Crime

How Two Sox Proteins Cooperate to Specify Arterial Fate

Suk-Won Jin, Cam Patterson

From the Carolina Cardiovascular Biology Center (S.-W.J., C.P.), Departments of Cell and Molecular Physiology (S.-W.J.) and Medicine (C.P.), the Curriculum in Genetics and Molecular Biology (S.-W.J.), School of Medicine, University of North Carolina at Chapel Hill.

Correspondence to Cam Patterson, MD, Director, Division of Cardiology and Carolina Cardiovascular Biology Center, University of North Carolina at Chapel Hill, 8200 Medical Biomolecular Research Building, Chapel Hill, NC 27599-7126; E-mail cpatters@med.unc.edu

See related article, pages 12–15

Key Words: arterial specification • Sox protein • zebrafish

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

Vertebrates have evolved 2 types of blood vessels—arteries and veins—that function to supply oxygen and nutrients and remove cellular waste. To efficiently accomplish these specialized functions, arteries and veins have developed distinct morphological and molecular differences. As a result, the endothelial cells that compose arteries and veins are vastly different in their biochemical and cellular properties. During development, the nascent endothelial cells generated from hemangioblasts or angioblasts^1,2 undergo tightly regulated specification and differentiation processes to adopt either the arterial or venous endothelial fate. Differentiated endothelial cells migrate and aggregate to form either arteries or veins according to their adopted fate.³ Dysregulation of these regulated events often results in devastating consequences. For instance, failure to segregate arterial and venous endothelial cells causes potentially fatal clinical conditions such as arteriovenous malformation, hereditary hemorrhagic telangiectasia, and cerebral cavernous malformation.⁴

Significant progress has been made in understanding how nascent endothelial cells adopt the arterial fate, resulting in identification of several key signaling molecules and their intracellular transducers involved in the specification of arterial endothelial cells.⁵ However, transcription factors that function downstream of these signaling cascades are largely unknown to date. Recently, hey2/Gridlock,^6,7 a member of the hairy and enhancer of split-related family of bHLH transcription factors, and Foxc1 and Foxc2,^8,9 which are forkhead transcription factors, have been implicated in arterial specification (Figure). A report in this issue of Circulation Research by Herpers et al elucidates the essential function of another transcription factor family, Sox, in this process.¹⁰

View larger version (15K):   Figure. Transcriptional regulation of arterial . . . [Full Text of this Article]

Related Article:

Redundant Roles for Sox7 and Sox18 in Arteriovenous Specification in Zebrafish

Robert Herpers, Esther van de Kamp, Henricus J. Duckers, and Stefan Schulte-Merker
Circ. Res. 2008 102: 12-15. [Abstract] [Full Text] [PDF]

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