Interstitial trophoblast invasion in the decidua and mesometrial triangle during the last third of pregnancy in the rat

Vercruysse, Lisbeth; Caluwaerts, Silvia; Luyten, C; Pijnenborg, Robert

doi:10.1016/j.placenta.2004.11.004

Cited by 115 publications

(107 citation statements)

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“…27,28 In rats, interstitial trophoblast cell invasion occurs after endovascular invasion. 25 This finding again supports our hypothesis that the observed vasculopathy occurred at the end of pregnancy, hampering physiological interstitial trophoblast cell invasion and a putative (according to Chakraborty et al 16 ) increased endovascular trophoblast cell invasion. The increased weight of the uteroplacental unit in anti-asialo GM1-treated preeclamptic rats and especially their increased uteroplacental unit/fetal weight ratio could reflect placental insufficiency as a consequence of decreased trophoblast cell invasion.…”

Section: Discussionsupporting

confidence: 85%

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Natural Killer Cell Reduction and Uteroplacental Vasculopathy

et al. 2016

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Abstract-Uterine natural killer cells are important for uteroplacental development and pregnancy maintenance. Their role in pregnancy disorders, such as preeclampsia, is unknown. We reduced the number of natural killer cells by administering rabbit anti-asialo GM1 antiserum in an established rat preeclamptic model (female human angiotensinogen×male human renin) and evaluated the effects at the end of pregnancy (day 21), compared with preeclamptic control rats receiving normal rabbit serum. In 100% of the antiserum-treated, preeclamptic rats (7/7), we observed highly degenerated vessel cross sections in the mesometrial triangle at the end of pregnancy. This maternal uterine vasculopathy was characterized by a total absence of nucleated/living cells in the vessel wall and perivascularly and prominent presence of fibrosis. Furthermore, there were no endovascular trophoblast cells within the vessel lumen. In the control, normal rabbit serum-treated, preeclamptic rats, only 20% (1/5) of the animals displayed such vasculopathy. We confirmed the results in healthy pregnant wild-type rats: after anti-asialo GM1 treatment, 67% of maternal rats displayed vasculopathy at the end of pregnancy compared with 0% in rabbit serum-treated control rats. This vasculopathy was associated with a significantly lower fetal weight in wild-type rats and deterioration of fetal brain/liver weight ratio in preeclamptic rats. Anti-asialo GM1 application had no influence on maternal hypertension and albuminuria during pregnancy. Our results show a new role of natural killer cells during hypertensive pregnancy in maintaining vascular integrity. In normotensive pregnancy, this integrity seems important for fetal growth. (Hypertension. 2016;68:964-973.

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Section: Discussionsupporting

confidence: 85%

“…In humans and rats, trophoblast cells invade the uterine interstitium 25,26 and the lumina of spiral arteries. 27,28 In rats, interstitial trophoblast cell invasion occurs after endovascular invasion.…”

Section: Discussionmentioning

confidence: 99%

Natural Killer Cell Reduction and Uteroplacental Vasculopathy

et al. 2016

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“…a Carter (27) reports that orangutan specimens were not available to determine whether orangutan invasion proceeds through the interstitial route, but Mossman (38), Benirschke (39), and Gruenwald (28) describe fetal invasion in orangutans as interstitial and/or very invasive. b There is some evidence for interstitial invasion in rats during the last part of pregnancy (40). and MER39 elements between the orangutan and OWM constructs (Fig.…”

mentioning

confidence: 99%

Transformation of a transposon into a derived prolactin promoter with function during human pregnancy

Emera

Wagner

2012

Proc. Natl. Acad. Sci. U.S.A.

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Transposable elements (TEs) are known to provide DNA for host regulatory functions, but the mechanisms underlying the transformation of TEs into cis-regulatory elements are unclear. In humans two TEs-MER20 and MER39-contribute the enhancer/ promoter for decidual prolactin (dPRL), which is dramatically induced during pregnancy. We show that evolution of the strong human dPRL promoter was a multistep process that took millions of years. First, MER39 inserted near MER20 in the primate/rodent ancestor, and then there were two phases of activity enhancement in primates. Through the mapping of causal nucleotide substitutions, we demonstrate that strong promoter activity in apes involves epistasis between transcription factor binding sites (TFBSs) ancestral to MER39 and derived sites. We propose a mode of molecular evolution that describes the process by which MER20/MER39 was transformed into a strong promoter, called "epistatic capture." Epistatic capture is the stabilization of a TFBS that is ancestral but variable in outgroup lineages, and is fixed in the ingroup because of epistatic interactions with derived TFBSs. Finally, we note that evolution of human promoter activity coincides with the emergence of a unique reproductive character in apes, highly invasive placentation. Because prolactin communicates with immune cells during pregnancy, which regulate fetal invasion into maternal tissues, we speculate that ape dPRL promoter activity evolved in response to increased invasiveness of ape fetal tissue.cis-regulatory evolution | human evolution | human pregnancy I n the pursuit to understand mechanisms underlying the evolution of gene regulation, it has become increasingly clear that transposable elements play a critical role in regulatory evolution by providing novel genetic elements, including new introns, promoters, enhancers, and insulators (1). In addition to individual examples showing that transposable elements (TEs) are associated with host regulatory function, computational work shows that TEs intersect with many promoter regions (2) and are overrepresented in predicted regulatory regions [(3, 4); see review by Feschotte (1)]. Many questions remain unanswered. How frequently are TEs actually co-opted for regulatory function? What is the adaptive significance of these events? Are TEs used by the host genome immediately upon insertion or do they require extensive sequence evolution before acquiring a biological role? What are the molecular changes that transform a transposable element into a cisregulatory element?In this paper we address the latter two questions posed above by investigating evolution of the decidual prolactin promoter in primates. In a recent paper we showed that the prolactin gene was independently recruited into uterine expression in primates, mice, and elephants by the co-option of different transposable elements, highlighting the frequency at which TEs can be recruited and their importance in gene regulatory innovation (5). Here we trace the evolutionary history and function of transposabl...

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“…Dams were monitored daily to ensure equivalent food consumption, and weighed weekly after E0. Fetuses and placentas were harvested for study on E19, because that point marks completion oftrophoblast cell invasion into decidua and spiral arteries [23]. Placental tissue with underlying mesometrial triangle was weighed, immersion fixed in Histochoice, and embedded in paraffin for histological sectioning [4].…”

Section: Gestational Ethanol Exposure Modelmentioning

confidence: 99%

“…Histological sections of placenta with underlying mesometrial triangle (5 µm thick) were immunostained with monoclonal antibody to Cytokeratin (CK) to detect invasive trophoblastic cells at the implantation site as previously described [5,23]. Briefly, deparaffinized and rehydrated tissue slides were incubated in preheated EnVision TM FLEX Target Retrieval Solution (high pH=9.0) for 20 minutes at 95-100°C.…”

Section: Immunohistochemistrymentioning

confidence: 99%

A Potential Administration-time Dependent Effect of Bevacizumab in Improving Overall Survival and Increasing Metastasis in Metastatic Colorectal Cancer

Zhang¹,

He²,

Zhou³

et al. 2013

Chemotherapy

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Background: One of the major adverse effects of maternal ethanol consumption is intrauterine growth restriction (IUGR). Previous studies demonstrated that ethanol-induced IUGR is mediated by impaired placentation. Chronic gestational ethanol exposure reduces trophoblastic cell motility and invasiveness through inhibition of insulin/IGF signaling leading to impaired vascular transformation at the implantation site. Furthermore, ethanol reduces the number of secondary giant cells that mediate vascular invasion in rat placenta. However, the degree to which ethanol inhibits progenitor cell survival and differentiation is not known.

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Interstitial trophoblast invasion in the decidua and mesometrial triangle during the last third of pregnancy in the rat

Cited by 115 publications

References 25 publications

Natural Killer Cell Reduction and Uteroplacental Vasculopathy

Natural Killer Cell Reduction and Uteroplacental Vasculopathy

Transformation of a transposon into a derived prolactin promoter with function during human pregnancy

A Potential Administration-time Dependent Effect of Bevacizumab in Improving Overall Survival and Increasing Metastasis in Metastatic Colorectal Cancer

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