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(Circulation Research. 2007;100:754.)
© 2007 American Heart Association, Inc.

Editorials

Physiological Smooth Muscle Cell Apoptosis Contributes to the Uterine Vascular Remodeling in Human Early Pregnancy

Jean-Jacques Helwig, Philippe Le Bouteiller

From the INSERM, Unit 727 (J.-J.H.), Strasbourg, France; Louis Pasteur University, Strasbourg, France; INSERM, Unit 563 (P.L.B.), Toulouse, France; Purpan Hospital, Toulouse, France.

Correspondence to Jean-Jacques Helwig, PhD, DrSci, Chief, INSERM U727, ULP-Faculté de Médecine, 11 rue Humann-Bat.4-, 1^eret, 67085 Strasbourg Cedex, France. E-mail jean-jacques.helwig@pharmaco-ulp.u-strasbg.fr.

See related article, pages 834–841

Key Words: spiral artery • placenta • death receptors • TRAIL

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

Although equipped with the entire machinery driving cell proliferation and cell death, the turnover of the vascular smooth muscle cell (VSMC) layer within the vascular wall is quite low throughout the adult normal body. Vascular wall remodeling with VSMC apoptosis is routinely considered as associated with vascular diseases. This includes the development and regression of vascular thickening in hypertension, in advanced atherosclerotic plaques where VSMC apoptosis promotes plaque rupture, after angioplasty-induced arterial injury, as well as in arterial aneurysm where apoptosis is responsible for excessive slackening and rupture of the vessel media.¹ Furthermore, in several animal studies, early pregnancy is a physiological situation where vessel wall remodeling plays a vital role. Indeed, in the first trimester of human pregnancy, vascular wall remodeling through degenerative changes converts the uterine spiral arteries located within the decidua basilis into toneless, widely opened arteries, thus enabling abundant blood supply to the maternal-fetal exchange area within the placenta. It is known that extravillous cytotrophoblasts deriving from fetal cytotrophoblastic shell migrate into segments of the spiral artery wall, through retrograde endovascular (intravasation) and interstitial migratory pathways (extravasation) into the decidua basilis to trigger the disappearance of endothelial and VSMC. In this process, trophoblasts become buried intramurally within a fibrinoid layer, which replaces the original muscular medial layer. Such trophoblast invasion converts the ends of spiral arteries into a wide caliber vessel that can better deliver maternal blood to the expanding intervillous space of the placenta (Figure 1A). Defective or incomplete trophoblast invasion can result . . . [Full Text of this Article]

Related Article:

Fetal-Derived Trophoblast Use the Apoptotic Cytokine Tumor Necrosis Factor-–Related Apoptosis-Inducing Ligand to Induce Smooth Muscle Cell Death

Rosemary J. Keogh, Lynda K. Harris, Abigail Freeman, Philip N. Baker, John D. Aplin, Guy StJ. Whitley, and Judith E. Cartwright
Circ. Res. 2007 100: 834-841. [Abstract] [Full Text] [PDF]