Vascular Changes in the Decidua Associated with Eclamptogenic Toxemia of Pregnancy

Zeek, Pearl M.; Assali, N.S.

doi:10.1093/ajcp/20.12.1099

Cited by 251 publications

(82 citation statements)

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“…trophoblast invasion of the spinal arterioles during the first half of pregnancy [2,3] and by decreased levels of circulating immunoregulatory cytokines, including IL10 [17,18]. However, it was previously reported that when IL10 is administered directly to villous explants, it functions as a negative regulator of trophoblast invasiveness, and that it decreases MMP9 expression in these tissues [30].…”

Section: Discussionmentioning

confidence: 99%

“…Preeclampsia is one of the most common causes of morbidity and mortality during pregnancy, and is associated with decreased trophoblast invasion and remodeling of the uterine spiral arterioles during the first half of pregnancy [1][2][3]. Because of this structural maladaptation, the spiral arterioles in pregnancies complicated with preeclampsia have reduced diameters and, due to the persistence of an intact endothelium and tunica media, they maintain their responsiveness to vasoactive molecules [4].…”

Section: Introductionmentioning

confidence: 99%

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Coordinated Regulation of Human Trophoblast Invasiveness by Macrophages and Interleukin 101

Renaud

Macdonald-Goodfellow

Graham

2007

Biology of Reproduction

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Trophoblast invasion and modification of the spiral arterioles are essential for the establishment of adequate uteroplacental blood flow during pregnancy. However, such vascular remodeling is deficient in preeclampsia. This disease is also associated with increased maternal levels of circulating proinflammatory cytokines such as tumor necrosis factor (TNF) and reduced levels of immunoregulatory cytokines such as interleukin 10 (IL10). We have previously shown that activated macrophages inhibit trophoblast invasiveness in vitro. The present study demonstrates that IL10 interferes with the invasion-inhibitory effect that activated macrophages exert on trophoblast cells. Co-culture experiments revealed that human lipopolysaccharide (LPS)-activated macrophages inhibited the ability of immortalized HTR-8/SVneo human trophoblast cells to invade through reconstituted extracellular matrix. This effect of activated macrophages on trophoblast invasiveness was paralleled by decreased expression of urokinase plasminogen activator receptor (PLAUR) on the surface of trophoblast cells, and by increased secretion of plasminogen activator inhibitor type 1 (SERPINE1). Exposure of LPS-treated macrophages to IL10 prior to co-culture prevented their ability to inhibit trophoblast invasion, PLAUR expression, and to stimulate SERPINE1 secretion. Interleukin 10 prevented macrophage activation by LPS as determined by the lack of secretion of TNF in the culture medium, and a neutralizing TNF antibody completely blocked the effect of macrophages on trophoblast invasion. These results indicate that decreased circulating levels of IL10 associated with preeclampsia may contribute to inadequate trophoblast invasion and remodeling of the uterine spiral arterioles.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Coordinated Regulation of Human Trophoblast Invasiveness by Macrophages and Interleukin 101

Renaud

Macdonald-Goodfellow

Graham

2007

Biology of Reproduction

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“…Acute atherosis is another prominent vascular alteration that is often observed in preeclampsia, and also in idiopathic intrauterine growth retardation [19, 20]. Such vasculopathy of the spiral arteries is defined by fibrinoid necrosis of the vessel wall, accumulation of lipid-laden macrophages, and a mononuclear perivascular infiltrate [21].…”

Section: Basic Pathology and Physiology Of Preeclampsiamentioning

confidence: 99%

The biology of preeclampsia

Kanasaki

Kalluri

2009

Kidney International

141

109

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Preeclampsia is a systemic disease that results from placental defects and occurs in about 5–8% of pregnancies worldwide. Preeclampsia is a disease of many theories, wherein investigators put forward their favorite mechanistic ideas, each with a causal appeal for the pathogenesis of preeclampsia. In reality, the patho-mechanism of preeclampsia remains largely unknown. Preeclampsia, as diagnosed in patients today, is likely a heterogeneous collection of disease entities that share some common features but also exhibit important differences. Therefore, one single mechanism may never be found to explain all the variants of preeclampsia. Current research must focus on evaluating such diverse mechanisms, as well as the possible common effectors pathways. Here we provide a discussion of several possible mechanisms and putative theories proposed for preeclampsia, with particular emphasis on the recent discovery of a new genetic mouse model offering new opportunities to explore experimental therapies.

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“…Originally described in preeclampsia, acute atherosis has also been found in other complications of pregnancy including spontaneous preterm labor (sPTL)/premature prelabor rupture of membrane (PPROM) [50], fetal death [50], gestational diabetes mellitus [5,15,24,50], gestational and chronic hypertension [15,24,27,28,50], systemic lupus erythematosus, and antiphospholipid antibody syndrome [14,24,31,34,37], intrauterine fetal growth restriction (IUGR) [13,16,19,20,22,32,50]. It is rarely observed in normal pregnancy [3,4,21,30,43,50]. The presence of acute atherosis has also been associated with a more severe form of preeclampsia [4,46,50].…”

Section: Introductionmentioning

confidence: 99%

Placental lesions associated with acute atherosis

Kim

Chaemsaithong

Romero

et al. 2014

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective Acute atherosis is a lesion of the spiral arteries characterized by fibrinoid necrosis of the vessel wall, an accumulation of fat-containing macrophages, and a mononuclear perivascular infiltrate, which can be found in patients with preeclampsia, fetal death, small-for-gestational age (SGA), spontaneous preterm labor/premature prelabor rupture of membrane, and spontaneous mid-trimester abortion. This lesion is thought to decrease blood flow to the intervillous space which may lead to other vascular lesions of the placenta. The objective of this study was to test whether there is an association between acute atherosis and placental lesions that are consistent with maternal vascular underperfusion, amniotic fluid infection, fetal vascular thrombo-occlusive disease or chronic inflammation. Material and methods A retrospective cohort study of pregnant women who delivered between July 1998 and July 2014 at Hutzel Women’s Hospital/Detroit Medical Center was conducted examine 16,457 placentas. The frequency of placenta lesions (diagnosed using the criteria of the Perinatal Section of the Society for Pediatric Pathology) was compared between pregnancies with and without atherosis. Results Among 16,457 women who were enrolled, 10.2% (1,671/16,457) were excluded, leaving 14,786 women who contributed data for analysis. Among them, the prevalence of acute atherosis was 2.2% (326/14,786). Women with acute atherosis were more than six times as likely as those without to have placental lesions consistent with maternal underperfusion (adjusted odds ratio- aOR: 6.7; 95% CI 5.2–8.6). To a lesser degree, acute atherosis was also associated with greater risks of having either lesions consistent with fetal vascular thrombo-occlusive disease (aOR 1.7; 95% CI 1.2–2.3) or chronic chorioamnionitis (aOR 1.9; 95% CI 1.3–3), but not with other chronic inflammatory lesions, after adjusting for gestational age at delivery. In contrast, women with acute atherosis were 60% less likely to have lesions consistent with amniotic fluid infecition, adjusting for gestational age at delivery (aOR 0.4; 95% CI 0.3–0.5). Conclusions Acute atherosis is associated with increased risks of having placental lesions consistent with maternal vascular underperfusion, and to a lesser extent, chronic chorioamnionitis and those consistent with fetal vascular thrombo-occlusive disease.

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Vascular Changes in the Decidua Associated with Eclamptogenic Toxemia of Pregnancy

Cited by 251 publications

References 0 publications

Coordinated Regulation of Human Trophoblast Invasiveness by Macrophages and Interleukin 101

Coordinated Regulation of Human Trophoblast Invasiveness by Macrophages and Interleukin 101

The biology of preeclampsia

Placental lesions associated with acute atherosis

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