Abstract
During the first twenty weeks of human pregnancy, extravillous trophoblasts (EVT) colonise the decidua and remodel the uterine spiral arteries as far as the first third of the myometrium. This process leads to an irreversible vasodilatation, ensuring that maximal blood flow is delivered to the materno-fetal interface at an optimal velocity for nutrient exchange. There is accumulating evidence that subtle changes in vascular structure precede EVT colonisation; however, full physiological transformation is only achieved in the presence of trophoblast. This review discusses the mechanisms employed to facilitate arterial dilatation, including recent data regarding the contribution of vascular cell apoptosis, the importance of elastin catabolism and the source of candidate elastases. It also examines how the complex interplay between EVT, endothelial cells, smooth muscle cells and decidual leukocytes (macrophages and uterine natural killer cells) leads to enhanced receptivity to invasion, vascular cell loss and extracellular matrix remodelling. © 2010 Elsevier Ltd. All rights reserved.
Original language | English |
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Pages (from-to) | S93-S98 |
Journal | Placenta |
Volume | 31 |
DOIs | |
Publication status | Published - Mar 2010 |
Keywords
- Apoptosis
- Artery
- Decidua
- Elastin
- EVT
- Extracellular matrix
- Invasion
- Leukocytes
- Macrophages
- Myometrium
- Remodelling
- Trophoblast
- Uterine natural killer cells
- Vascular smooth muscle