The relation of increased uterine artery blood flow resistance and impaired trophoblast invasion in pre-eclamptic pregnancies

Güzin, Kadir; Tomruk, Sedat; Tunçay, Yıldız Ayhan; Naki, Murat; Sezginsoy, Selen; Zemherı, Ebru; Yücel, Neşe; Kanadikirik, Fahrettin

doi:10.1007/s00404-005-0005-2

Cited by 57 publications

(35 citation statements)

References 14 publications

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“…High resistance uterine artery indices were previously found to correlate with decreased endovascular trophoblast invasion of decidual spiral arteries [48]. This finding is consistent with the correlation between high uterine artery resistance index and decreased endovascular trophoblast invasion of decidual and myometrial spiral arteries in women with preeclampsia [49]. In the first trimester decidual tissues from pregnancies with high uterine artery index, Cartwright et al identified perturbed gene expression and aberrant dNK cell phenotype, as well as impaired regulation of trophoblast function by dNK cells in vitro [35].…”

Section: Decidual Gene Expression and Function Before Onset Of Clinicsupporting

confidence: 84%

Emerging role for dysregulated decidualization in the genesis of preeclampsia

2017

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In normal human placentation, uterine invasion by trophoblast cells and subsequent spiral artery remodeling depend on cooperation among fetal trophoblasts and maternal decidual, myometrial, immune and vascular cells in the uterine wall. Therefore, aberrant function of anyone or several of these cell-types could theoretically impair placentation leading to the development of preeclampsia. Because trophoblast invasion and spiral artery remodeling occur during the first half of pregnancy, the molecular pathology of fetal placental and maternal decidual tissues following delivery may not be informative about the genesis of impaired placentation, which transpired months earlier. Therefore, in this review, we focus on the emerging prospective evidence supporting the concept that deficient or defective endometrial maturation in the late secretory phase and during early pregnancy, i.e., pre-decidualization and decidualization, respectively, may contribute to the genesis of preeclampsia. The first prospectively-acquired data directly supporting this concept were unexpectedly revealed in transcriptomic analyses of chorionic villous samples (CVS) obtained during the first trimester of women who developed preeclampsia 5 months later. Additional supportive evidence arose from investigations of Natural Killer cells in first trimester decidua from elective terminations of women with high resistance uterine artery indices, a surrogate for deficient trophoblast invasion. Last, circulating insulin growth factor binding protein-1, which is secreted by decidual stromal cells was decreased during early pregnancy in women who developed preeclampsia. We conclude this review by making recommendations for further prospectively-designed studies to corroborate the concept of endometrial antecedents of preeclampsia. These studies could also enable identification of women at increased risk for developing preeclampsia, unveil the molecular mechanisms of deficient or defective (pre)decidualization, and lead to preventative strategies designed to improve (pre)decidualization, thereby reducing risk for preeclampsia development.

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Section: Decidual Gene Expression and Function Before Onset Of Clinicsupporting

confidence: 84%

Emerging role for dysregulated decidualization in the genesis of preeclampsia

2017

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“…[100] In another study, myometrial spiral artery invasion was absent in 6 of 12 mild preeclamptics with a mean gestational age of 37 weeks and in 15 of 20 severe preeclamptics with a mean gestational age of 34 weeks. [101] Similarly, spiral artery vascular remodeling was abnormal not only in all 21 cases of preeclampsia with FGR but also in 8 of 9 cases of preeclampsia without FGR. [102] In a study of myometrial spiral artery remodeling, it was absent in 1 of 26 normal pregnancies, 7 of 11 preeclamptics with FGR, and 6 of 22 preeclamptics without FGR.…”

Section: Subsets Of Preeclampsiamentioning

confidence: 99%

The placenta in preeclampsia

Roberts

Escudero

2012

Pregnancy Hypertension: An International Journal of Women's Car

340

249

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The root cause of preeclampsia is the placenta. Preeclampsia begins to abate with the delivery of the placenta and can occur in the absence of a fetus but with the presence of trophoblast tissue with hydatidiform moles. In view of this, study of the placenta should provide insight into the pathophysiology of preeclampsia. In this presentation we examine placental pathological and pathophysiological changes with preeclampsia and fetal growth restriction (FGR). It would seem that this comparison should be illuminating as both conditions are associated with similarly abnormal placentation yet only in preeclampsia is there a maternal pathophysiological syndrome. Similar insights about early and late onset preeclampsia should also be provided by such information. We report that the placental abnormalities in preeclampsia are what would be predicted in a setting of reduced perfusion and oxidative stress. However, the differences from FGR are inconsistent. The most striking differences between the two conditions are found in areas that have been the least studied. There are differences between the placental findings in early and late onset preeclampsia but whether these are qualitative, indicating different diseases, or simply quantitative differences within the same disease is difficult to determine. We attempt to decipher the true differences, seek an explanation for the disparate results and provide recommendations that we hope may help resolve these issues in future studies.

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“…This segment retains a hypertrophic muscular structure, although interstitial trophoblasts are present, sometimes in excessive numbers (3). The defective transformation is more severe in the myometrial, than in the decidual, segments (8, 29). …”

Section: Introductionmentioning

confidence: 99%

The “Great Obstetrical Syndromes” are associated with disorders of deep placentation

Brosens

Pijnenborg

Vercruysse

et al. 2011

American Journal of Obstetrics and Gynecology

1,227

973

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Defective deep placentation has been associated with a spectrum of complications of pregnancy including preeclampsia, intrauterine growth restriction, preterm labor, preterm premature rupture of membranes, late spontaneous abortion and abruption placentae. The disease of the placental vascular bed that underpins these complications is commonly investigated with targeted biopsies. In this review, we critically evaluate the biopsy technique to summarize the salient types of defective deep placentation and propose criteria for the classification of defective deep placentation into 3 types based on the degree of restriction of remodelling and the presence of obstructive lesions in the myometrial segment of the spiral arteries.

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The relation of increased uterine artery blood flow resistance and impaired trophoblast invasion in pre-eclamptic pregnancies

Abstract: Doppler ultrasonography is not only a non-invasive method for evaluating fetal status in pre-eclamptic pregnancies, but it also correlates with partial trophoblastic invasion in spiral arteries, which contributes to the pathophysiologic mechanisms involved in pre-eclampsia.

Cited by 57 publications

References 14 publications

Emerging role for dysregulated decidualization in the genesis of preeclampsia

Emerging role for dysregulated decidualization in the genesis of preeclampsia

The placenta in preeclampsia

The “Great Obstetrical Syndromes” are associated with disorders of deep placentation

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