Abnormal Placentation in Preeclampsia

8/10/2019 Abnormal Placentation in Preeclampsia

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Abnormal placentation in preeclampsia. In normal placental development, invasive

cytotrophoblasts of fetal origin invade the maternal spiral arteries, transforming

them from small-caliber resistance vessels to high-caliber capacitance vessels

capable of providing placental perfusion adequate to sustain the growing fetus.

During the process of vascular invasion, the cytotrophoblasts dierentiate from an

epithelial phenotype to an endothelial phenotype, a process referred to aspseudovasculogenesis, or vascular mimicry (top. In preeclampsia, cytotrophoblasts

fail to adopt an invasive endothelial phenotype. Instead, invasion of the spiral

arteries is shallow, and they remain small-caliber resistance vessels (bottom.

!igure reproduced with permission from "am et al.#$


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s!lt% and soluble endoglin (s&ng cause endothelial dysfunction by antagoni'ing

vascular endothelial growth factor (&)! and transforming growth factor-*% (+)!-

*% signaling. +here is mounting evidence that &)! and +)!-*% are required to

maintain endothelial health in several tissues including the idney and perhaps the

placenta. During normal pregnancy, vascular homeostasis is maintained by

physiological levels of &)! and +)!-*% signaling in the vasculature. Inpreeclampsia, ecess placental secretion of s!lt% and s&ng ( endogenous

circulating antiangiogenic proteins inhibits &)! and +)!-*% signaling,

respectively, in the vasculature. +his results in endothelial cell dysfunction,

including decreased prostacyclin, nitric oide production, and release of

procoagulant proteins. +*/II indicates transforming growth factor-* type II receptor.

0ummary of the pathogenesis of preeclampsia. Angiotensin II +ype I /eceptor

Activating Autoantibodies (A+%-AA, immunologic factors, oidative stress, and otherfactors (such as decreased heme oygenase epression may cause placental

dysfunction, which in turn leads to the release of antiangiogenic factors (such as

s!lt% and soluble endoglin 1s&ng2 and other in3ammatory mediators to induce

preeclampsia. 45 indicates natural iller6 7+4, hypertension.


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8reeclampsia is a ma9or contributor to the maternal and neonatal mortality and

morbidity.%,It is the nd largest cause of maternal mortality worldwide and aects

$: to ;: of pregnant women worldwide. wees of gestation in a previously normotensive

woman,


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+he diagram represents the early development of the trophoblast lineage. +he

decisive dierentiation steps are highlighted with gray boes. +he dar gray boes

indicate the very early dierentiation steps. If there is a failure during this time of

development the pregnancy may result in a combination of preeclampsia (8& and

IE)/. If only the villous pathway is aected, it may result in a preeclampsia (lower

left. And if only the etravillous pathway is aected it may result in an IE)/ (lower

right.


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1. Normal PregnancyDuring normal pregnancy aged and late apoptotic syncytiotrophoblast nuclei arepaced into apical protrusions of the syncytiotrophoblast,


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occurs after midgestation. +his discrepancy can be eplained as follows During the=rst trimester of pregnancy trophoblast turnover is dierent to the turnover later ingestation. In the =rst trimester most of the fusion events of cytotrophoblast cellswith the syncytiotrophoblast are needed for growth of the syncytiotrophoblastrather than for the maintenance of this layer.

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Abnormal Placentation in Preeclampsia