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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1934-1935
doi: 10.1161/01.ATV.0000236220.06886.e3
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1934.)
© 2006 American Heart Association, Inc.


Editorials

Arteries or Veins?

VEGF Helps EPCs Choose Their cAMP

Jean-Sébastien Silvestre; Ziad Mallat

From Inserm U689, Centre de Recherche Cardiovasculaire Lariboisière, Paris, France.

Correspondence to Ziad Mallat, Inserm U689, Centre de Recherche Cardiovasculaire Lariboisière, 41 Bd de la Chapelle, 75010 Paris, France. E-mail mallat@larib.inserm.fr


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

Blood vessels are initially formed by a process termed vasculogenesis, which denotes the in situ differentiation of vascular progenitor cells into endothelial cells and their organization into primary vessels.1 As vessels begin a remodeling process, they undergo localized proliferation and regression, as well as programmed branching and migration. One of the first events that takes place with the onset of circulation is the specification of arteries versus veins.

See page 1977

Until recently, arterial versus venous fate was known as a late event in the vascular development process, resulting from hemodynamic flow differences between the two types of vessels.2 However, specific markers for arteries and veins were discovered, which labeled endothelial cells from early developmental stages onwards, before the assembly of any vascular wall. For the arterial system, ephrinB2, neuropilin 1, and members of the Notch pathway appear to play critical roles.2 Other molecules such as EphB4 or neuropilin-2 are specifically expressed in the venous system. The expression of these markers is segregated to the future arterial and venous parts of the primitive vascular network despite the absence of flow, suggesting that arterial and venous fate is established in early progenitors. The notch signaling pathway has been implicated as a prime player in arterial versus venous switch. Administration of a dominant-negative form of Suppressor of Hairless (the major downstream effector of Notch signaling) resulted in decreased expression of arterial markers, whereas expression of an activated notch construct induced ectopic arterial markers in the vein system.3,4 This arterial–venous decision is guided, . . . [Full Text of this Article]


Related Article:

Adrenomedullin/Cyclic AMP Pathway Induces Notch Activation and Differentiation of Arterial Endothelial Cells From Vascular Progenitors
Takami Yurugi-Kobayashi, Hiroshi Itoh, Timm Schroeder, Akiko Nakano, Genta Narazaki, Fumiyo Kita, Kentoku Yanagi, Mina Hiraoka-Kanie, Emi Inoue, Toshiaki Ara, Takashi Nagasawa, Ursula Just, Kazuwa Nakao, Shin-Ichi Nishikawa, and Jun K. Yamashita
Arterioscler Thromb Vasc Biol 2006 26: 1977-1984. [Abstract] [Full Text] [PDF]