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. 2012 Jan;5(1):9–18. doi: 10.1242/dmm.008516

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© 2012. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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Fig. 1. — Invasion defects in preeclampsia. (A) In a normal placenta, extravillous cytotrophoblast (ECTB) cells (green) move into the decidua (endometrium) and myometrium via interstitial invasion. Some ECTB cells enter maternal spiral arteries and replace the endothelial cells of the vessel walls, becoming endovascular ECTB (eECTB) cells, increasing vessel compliance and maximizing blood flow into placental blood spaces. (B) In the placenta of a preeclamptic patient, interstitial invasion is shallow and limited, with many ECTB cells in the basal plate remaining attached to anchoring villi (AV). Endovascular invasion is nearly absent, and spiral arterioles remain ‘stiff’. FV, floating villi. Image courtesy of The Curators of the University of Missouri (2011), a public corporation.