Quantitative differences in arterial morphometry define the placental bed in preeclampsia

Starzyk, Kathryn; Salafia, Carolyn M.; Pezzullo, John C.; Lage, Janice M.; Parkash, Vinita; Vercruysse, Lisbeth; Hanssens, Myriam; Pijnenborg, Robert

doi:10.1016/s0046-8177(97)90135-0

Cited by 51 publications

(29 citation statements)

References 9 publications

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“…This was revealed by a greater number of cross sections per artery, as has also recently been reported by others [14]. There are two different patterns of trophoblast behaviour in the defective placentation that occurs in preeclampsia.…”

Section: Discussionsupporting

confidence: 80%

Aberrant positioning of trophoblast and lymphocytes in the feto-maternal interface with pre-eclampsia

Stallmach

Hebisch

et al. 1999

Virchows Archiv

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Pregnancy represents the growth of an allograft where fetal trophoblast cells evade immune rejection and invade maternal tissue. There should be a balance between fetal trophoblast and maternal immune-responsive cells and alterations in the proportion of these cells may relate to pregnancy disorders. To test this, the decidual tissue of placental bed biopsies was examined and trophoblast cells and lymphocytes were quantified morphometrically; spiral arteries were classified as unchanged, transformed or affected by acute atherosis. Normal pregnancy (n=19) was characterized by the transformation of about one half of all spiral arteries within the placental bed. We found that 40% of all lymphocytes were CD56+ uterine NK cells and 60%, CD3+ T-lymphocytes; about 30% of these were CD8+ T cells. Intrauterine growth retardation in the context of preeclampsia (n=15) was accompanied by reduced trophoblast numbers within smaller and more tortuous arteries and an increase in the proportion of CD56+ uterine NK cells and CD8+ T lymphocytes in the decidua (70% of all CD3+ cells). In the case of pre-eclampsia without fetal growth retardation (n=14) no increase in CD56+ uterine NK cells was seen, while CD8+ T lymphocytes were significantly increased compared with the normal level (50% of all CD3+ cells). Fetal growth retardation is associated with poor transformation of spiral arteries and characterized by an increase of uterine NK cells. Symptoms of pre-eclampsia are independently associated with an increase in the cytotoxic T subset of decidual lymphocytes. Pre-eclampsia and related fetal growth retardation are seemingly caused by an enhancement of the maternal cytotoxic defence against the fetal allograft.

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Section: Discussionsupporting

confidence: 80%

Aberrant positioning of trophoblast and lymphocytes in the feto-maternal interface with pre-eclampsia

Stallmach

Hebisch

et al. 1999

Virchows Archiv

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“…Migrating trophoblasts transform the maternal spiral arterioles that supply maternal blood to the placenta from small caliber resistance vessels to large caliber capacitance vessels, allowing adequate maternal blood flow to the placenta (Starzyk et al 1997, Lyall 2005. The epidermal growth factor was reported to induce syncytialization of cytotrophoblasts and the secretion of human chorionic gonadotropin and human placental lactogen in vitro (Morrish et al 1987).…”

Section: Discussionmentioning

confidence: 99%

Role of extracellular signal-regulated kinase and AKT cascades in regulating hypoxia-induced angiogenic factors produced by a trophoblast-derived cell line

Fujita¹,

Tanabe²,

Sekijima³

et al. 2010

Journal of Endocrinology

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During human pregnancy, trophoblasts play an important role in embryo implantation and placental development. Cytotrophoblast cells invade the uterine spiral arteries and differentiate into extravillous trophoblasts, resulting in the remodeling of the uterine vessels and fetoplacental vasculature. During early pregnancy, a physiologically hypoxic environment induces the production of angiogenic factors, such as vascular endothelial growth factor (VEGF), which are suggested to locally control the vascular remodeling. Endoglin, a cell-surface coreceptor for transforming growth factor-b1, is highly expressed in endothelial cells and syncytiotrophoblasts, and can be associated with endothelial nitric oxide synthase and vascular homeostasis. Several studies have recently suggested that some pregnancy-related complications, such as preeclampsia, have their origins early in pregnancy as a result of abnormalities in implantation and placental development. Although angiogenic factors are recognized as key molecules in placental development, little is known about the mechanism(s) of their regulation in trophoblasts. In this study, we elucidated the mechanisms underlying the regulation of VEGF and endoglin production under hypoxic conditions in the trophoblast-derived cell line, BeWo. We evaluated the role of the AKT-MTOR cascade and ERK kinase in the expression of VEGF and endoglin in response to hypoxia using various kinase inhibitors and small interfering RNA targeted against hypoxia-inducible factor (HIF)-1a (listed as HIF1A in Hugo Database). Our results suggest that both the phosphatidylinositol 3-kinase-AKT-MTOR-HIF-1a and ERK-HIF-1a signaling pathways are crucial for increasing VEGF and endoglin expression in response to hypoxia in BeWo cells.

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“…Spiral and basal arteries from preeclamptic patients are more tortuous or densely distributed with narrower lumens and thicker walls than those from normal pregnancies [22,29,30]. These vessels may be more vulnerable to endothelial damage induced by hemodynamic stress, as in preeclampsia [31]. The possibility that damaged basal plate surface areas are repaired by endothelial cells recruited from circulating maternal endothelial progenitor cells is supported by the observation of Luppi et al [32].…”

Section: Discussionmentioning

confidence: 98%

Genetic origin and proportion of basal plate surface-lining cells in normal and abnormal pregnancies

Richani¹,

Romero

Soto³

et al. 2007

Human Pathology

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The human placenta is a transient organ, the villous surface of which is in direct contact with the maternal circulation during pregnancy. Thus, the syncytiotrophoblast and the basal plate-lining cells are considered continuous with the endothelial layer of the maternal vasculature. Two types of cells are found on the surface of the basal plate: trophoblasts (of fetal origin) and endothelial cells of putative maternal origin. Histologic abnormalities have been described in the basal plate of the placenta obtained from patients with preeclampsia and intrauterine growth restriction. Moreover, endothelial cell dysfunction and intravascular inflammation are key features of preeclampsia. The objectives of this study were to: (1) determine the origin of the endothelial cells located in the basal plate surface of the placenta (from male fetuses); and (2) analyze the relative proportion of the intervillous surface of the basal plate occupied by trophoblasts and endothelial cells. Immunohistochemistry and morphometry were performed in placentas from women in the following clinical groups: (1) normal-term pregnancies (n = 15); (2) severe preeclampsia at term (n = 15); (3) small-for-gestational-age (SGA) neonates delivered at term (n = 15); (4) preterm deliveries (<37 weeks) without inflammation (n = 5); and (5) preterm preeclampsia (n = 5). Laser capture microdissection and polymerase chain reaction were used to determine the allelic pattern of the amelogenin gene of the endothelial cells on the intervillous surface of the basal plate. Our results showed that: (1) the endothelial cells lining the basal plate in placentas of male fetuses were uniformly of maternal origin; and (2) in placentas from uncomplicated pregnancies, the median proportion of trophoblasts and endothelial cells covering the surface of the basal plate were 27.7% and 46.5%, respectively. The remaining area of the intervillous surface of the basal plate was composed of fibrin and anchoring villi. Of interest, placentas from women who delivered an SGA neonate had a higher proportion of trophoblasts and a lower proportion of endothelial cells lining the basal plate than those from normal pregnancies (P < .05). The same tendency was observed in placentas from patients with preeclampsia. This study demonstrates that endothelial cells of maternal origin cover the intervillous surface of the basal plate of the placenta, along with trophoblasts of fetal origin. The proportion of this surface lined by trophoblasts is greater in placentas from SGA and preeclampsia than in normal pregnancy. We propose that this change reflects a compensatory mechanism whereby the basal plate surface covered by injured endothelial cells is replaced by trophoblasts or results from a failure of trophoblastic involution in abnormal pregnancies. Our observations also suggest that the lining of the basal plate can provide information about the pathology of endothelial cells in complications of pregnancy.

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Quantitative differences in arterial morphometry define the placental bed in preeclampsia

Cited by 51 publications

References 9 publications

Aberrant positioning of trophoblast and lymphocytes in the feto-maternal interface with pre-eclampsia

Aberrant positioning of trophoblast and lymphocytes in the feto-maternal interface with pre-eclampsia

Role of extracellular signal-regulated kinase and AKT cascades in regulating hypoxia-induced angiogenic factors produced by a trophoblast-derived cell line

Genetic origin and proportion of basal plate surface-lining cells in normal and abnormal pregnancies

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