Talk:Placenta - Maternal Decidua

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Vascular endothelial expression of indoleamine 2,3-dioxygenase 1 forms a positive gradient towards the veto-maternal interface

PLoS One. 2011;6(7):e21774. doi: 10.1371/journal.pone.0021774. Epub 2011 Jul 6.

Blaschitz A, Gauster M, Fuchs D, Lang I, Maschke P, Ulrich D, Karpf E, Takikawa O, Schimek MG, Dohr G, Sedlmayr P. Source Institute of Cell Biology, Histology and Embryology, Center for Molecular Medicine, Medical University of Graz, Graz, Austria.

Abstract

We describe the distribution of indoleamine 2,3-dioxygenase 1 (IDO1) in vascular endothelium of human first-trimester and term placenta. Expression of IDO1 protein on the fetal side of the interface extended from almost exclusively sub-trophoblastic capillaries in first-trimester placenta to a nearly general presence on villous vascular endothelia at term, including also most bigger vessels such as villous arteries and veins of stem villi and vessels of the chorionic plate. Umbilical cord vessels were generally negative for IDO1 protein. In the fetal part of the placenta positivity for IDO1 was restricted to vascular endothelium, which did not co-express HLA-DR. This finding paralleled detectability of IDO1 mRNA in first trimester and term tissue and a high increase in the kynurenine to tryptophan ratio in chorionic villous tissue from first trimester to term placenta. Endothelial cells isolated from the chorionic plate of term placenta expressed IDO1 mRNA in contrast to endothelial cells originating from human umbilical vein, iliac vein or aorta. In first trimester decidua we found endothelium of arteries rather than veins expressing IDO1, which was complementory to expression of HLA-DR. An estimation of IDO activity on the basis of the ratio of kynurenine and tryptophan in blood taken from vessels of the chorionic plate of term placenta indicated far higher values than those found in the peripheral blood of adults. Thus, a gradient of vascular endothelial IDO1 expression is present at both sides of the feto-maternal interface. PMID 21755000

Cytotrophoblast induction of arterial apoptosis and lymphangiogenesis in an in vivo model of human placentation

J Clin Invest. 2006 Oct;116(10):2643-52. Epub 2006 Sep 21.

Red-Horse K, Rivera J, Schanz A, Zhou Y, Winn V, Kapidzic M, Maltepe E, Okazaki K, Kochman R, Vo KC, Giudice L, Erlebacher A, McCune JM, Stoddart CA, Fisher SJ.

Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, California, USA.

Abstract

We studied the vascular effects of invasive human cytotrophoblasts in vivo by transplanting placental villi to the fifth mammary fat pads or beneath the kidney capsules of Scid mice. Over 3 weeks, robust cytotrophoblast invasion was observed in both locations. The architecture of the mammary fat pad allowed for detailed analysis of the cells' interactions with resident murine blood vessels, which revealed specific induction of apoptosis in the endothelial cells and smooth muscle walls of the arterioles. This finding, and confirmation of the results in an in vitro coculture model, suggests that a parallel process is important for enabling cytotrophoblast endovascular invasion during human pregnancy. Cytotrophoblast invasion of the kidney parenchyma was accompanied by a robust lymphangiogenic response, while in vitro, the cells stimulated lymphatic endothelial cell migration via the actions of VEGF family members, FGF, and TNF-alpha. Immunolocalization analyses revealed that human pregnancy is associated with lymphangiogenesis in the decidua since lymphatic vessels were not a prominent feature of the nonpregnant endometrium. Thus, the placenta triggers the development of a decidual lymphatic circulation, which we theorize plays an important role in maintaining fluid balance during pregnancy, with possible implications for maternal-fetal immune cell trafficking. Comment in Literature watch. Cytotrophoblast induction of arterial apoptosis and lymphangiogenesis in an in vivo model of human placentation. [Lymphat Res Biol. 2006]

PMID 16998586

2013

IFPA Award in Placentology Lecture: Preeclampsia, the decidual battleground and future maternal cardiovascular disease

Placenta. 2013 Dec 18. pii: S0143-4004(13)00862-X. doi: 10.1016/j.placenta.2013.12.003.

Staff AC1, Redman CW2. Author information

Abstract

The decidua basalis is one of the frontiers between placenta and mother. Its spiral arteries ensure that the placenta and fetus have adequate access to the maternal circulation, without compromising maternal health. Normally this requires a tightly regulated collaboration between tissues of genetically different individuals. But like all frontiers it can become a battlefield. The decidua is difficult to sample systematically. Some of the problems have been resolved by our vacuum suction method. We review the technique and how it has contributed to what we know of decidual tissue, especially when it becomes a battlefield in preeclampsia, with its increased oxidative stress and inflammation. Acute atherosis is a poorly studied decidual lesion of late pregnancy, which mainly affects the decidual tips of spiral arteries in preeclampsia. It is characterized by lipid-filled foam cells and resembles early atherosclerosis. Poorly remodelled spiral arteries seem to be especially susceptible. The underlying mechanisms are largely unknown, but are likely to be similar to those of atherosclerosis and primarily the consequence of vascular inflammation. Acute atherosis also occurs in other pregnancy complications, even in normal pregnancies. It appears not to be confined to maladapted spiral arteries nor be caused by hypertension. It is important that foam cells result from inflammatory stimulation of macrophages. Hence, we propose that decidual inflammation of multiple causes underlies acute atherosis, with or without preeclampsia. Women suffering from preeclampsia have an augmented risk of cardiovascular disease later in life and of premature death. Acute atherosis may more specifically identify those women at augmented risk for such later cardiovascular disorders, whether or not it is associated with preeclampsia. Copyright © 2014 Elsevier Ltd. All rights reserved. KEYWORDS: Atherosclerosis, Atherosis, Cardiovascular disease, Hypertension, Preeclampsia, Pregnancy, Spiral artery

PMID 24411701

2012

Decidual macrophages and their roles at the maternal-feral interface

Yale J Biol Med. 2012 Mar;85(1):105-18. Epub 2012 Mar 29.

Houser BL.

Abstract

The semi-allogeneic fetus, whose genome consists of maternally and paternally inherited alleles, must coexist with an active maternal immune system during its 9 months in utero. Macrophages are the second most abundant immune cell at the maternal-fetal interface, although populations and functions for these populations remain ill defined. We have previously reported two distinct subsets of CD14(+) decidual macrophages found to be present in first trimester decidual tissue, 20 percent CD11c(HI) and 68 percent CD11c(LO). Interestingly, CD11c(HI) decidual macrophages express genes associated with lipid metabolism, inflammation, and antigen presentation function and specifically upregulate CD1 molecules. Conversely, CD11c(LO) decidual macrophages express genes associated with extracellular matrix formation, muscle regulation, and tissue growth. The large abundance of CD11c(HI) decidual macrophages and their ability to process antigens more efficiently than CD11c(LO) macrophages suggests that CD11c(HI) macrophages may be important antigen processing and presenting cells at the maternal-fetal interface, while CD11c(LO) macrophages may perform necessary homeostatic functions during placental construction. Thus, macrophage heterogeneity may be an important and necessary division of labor that leads to both an induction of maternal immune cell tolerance to fetal antigens as well as basic homeostatic functions in human pregnancy. KEYWORDS: NK cells; antigen presenting cells; lipids; macrophages; pregnancy; reproduction

PMID 22461749

Disordered IL-33/ST2 activation in decidualizing stromal cells prolongs uterine receptivity in women with recurrent pregnancy loss

PLoS One. 2012;7(12):e52252. doi: 10.1371/journal.pone.0052252. Epub 2012 Dec 27.

Salker MS, Nautiyal J, Steel JH, Webster Z, Sućurović S, Nicou M, Singh Y, Lucas ES, Murakami K, Chan YW, James S, Abdallah Y, Christian M, Croy BA, Mulac-Jericevic B, Quenby S, Brosens JJ. Author information

Abstract

Decidualization renders the endometrium transiently receptive to an implanting blastocyst although the underlying mechanisms remain incompletely understood. Here we show that human endometrial stromal cells (HESCs) rapidly release IL-33, a key regulator of innate immune responses, upon decidualization. In parallel, differentiating HESCs upregulate the IL-33 transmembrane receptor ST2L and other pro-inflammatory mediators before mounting a profound anti-inflammatory response that includes downregulation of ST2L and increased expression of the soluble decoy receptor sST2. We demonstrate that HESCs secrete factors permissive of embryo implantation in mice only during the pro-inflammatory phase of the decidual process. IL-33 knockdown in undifferentiated HESCs was sufficient to abrogate this pro-inflammatory decidual response. Further, sequential activation of the IL-33/ST2L/sST2 axis was disordered in decidualizing HESCs from women with recurrent pregnancy loss. Signals from these cultures prolonged the implantation window but also caused subsequent pregnancy failure in mice. Thus, Il-33/ST2 activation in HESCS drives an autoinflammatory response that controls the temporal expression of receptivity genes. Failure to constrain this response predisposes to miscarriage by allowing out-of-phase implantation in an unsupportive uterine environment.

PMID 23300625

Endometrial Receptivity Defects and Impaired Implantation in Diabetic NOD Mice

Biol Reprod. 2012 Apr 25. [Epub ahead of print]

Albaghdadi AJ, Kan FW.

Abstract Implantation failure is a major hurdle to a successful pregnancy. The high rate of post-implantation fetal loss in non-obese diabetic (NOD) mice is believed related to an abnormal decidual production of IFNgamma. To address whether diabetes alters the natural events associated with successful implantation, certain morphological and molecular features of uterine receptivity in diabetic NOD (dNOD) mice were examined in the normally mated pregnancy and in Concanavalin A (ConA)-induced pseudopregnancy. As opposed to normoglycemic NOD (cNOD) mice, dNOD mice expressed retarded maturation of their uterine pinopodes and over expressed MUC1 mucin at implantation sites (P < 0.001). Uterine production of Leukemia Inhibitory Factor (LIF) and the phosphorylation of uterine NFKBp65 and STAT3-Ty705 were found to be low (P < 0.01) during day 4.5 postcoitum, whereas IFNgamma was aberrantly over-expressed. Loss of temporal regulation of progesterone receptor (PR) A (PR A) and PR B, together with an aberrantly increased expression of the protein inhibitor of activated STAT-y (PIASy) (P < 0.01), and reduced recruitment (P < 0.01) of the latter to nuclear progesterone receptor sites were prominent features of decidualization failure occurring at peri-implantation in dNOD mice. In conclusion, the aberrant expression of endometrial IFNgamma in dNOD mice is associated with a non-receptive endometrial milieu contributing to peri-implantation embryo loss in type 1 diabetes.

PMID 22539679

The complement system at the embryo implantation site: friend or foe?

Front Immunol. 2012;3:55. Epub 2012 Mar 19.

Bulla R, Bossi F, Tedesco F. Source Department of Life Sciences, University of Trieste Trieste, Italy.

Abstract

An inflammatory-like process and vascular remodeling represent the main changes that occur in decidua in the early phase of pregnancy. These changes are partly induced by trophoblast cells that colonize the decidua and are also contributed by the complement system, which can easily be activated as a result of tissue remodeling. Local control by several complement regulators including surface-bound and soluble molecules is critical to prevent complement-mediated tissue damage in normal pregnancy. C7 expressed on the endothelial cells (ECs) surface has been recognized as a novel complement regulator involved in the control of the proinflammatory effect of the terminal complement complex. The protective role of placental complement regulators in pregnancy is underscored by the recent finding of an association of preeclampsia with mutations in the genes encoding for some of these proteins. Complement components produced at feto-maternal interface serve an important function in placental development. C1q synthesized by decidual ECs and expressed on the cell surface is particularly important in this regard because it acts as a molecular bridge between endovascular trophoblast and ECs. C1q is also produced by extravillous trophoblast and is used to favor trophoblast migration through the decidua. Defective expression of C1q by trophoblast is associated with impaired trophoblast invasion of decidua and may have important implications in pregnancy disorders such as preeclampsia characterized by reduced vascular remodeling.

PMID 22566936

http://www.frontiersin.org/Molecular_Innate_Immunity/10.3389/fimmu.2012.00055/abstract

maternal blood vessel EM image

2011

Leukemia inhibitory factor enhances endometrial stromal cell decidualization in humans and mice

PLoS One. 2011;6(9):e25288. Epub 2011 Sep 23.

Shuya LL, Menkhorst EM, Yap J, Li P, Lane N, Dimitriadis E. Source Embryo Implantation Laboratory, Prince Henry's Institute, Clayton, Melbourne, Australia.

Abstract

Adequate differentiation or decidualization of endometrial stromal cells (ESC) is critical for successful pregnancy in humans and rodents. Here, we investigated the role of leukemia inhibitory factor (LIF) in human and murine decidualization. Ex vivo human (H) ESC decidualization was induced by estrogen (E, 10(-8) M) plus medroxyprogesterone acetate (MPA, 10(-7) M). Exogenous LIF (≥50 ng/ml) induced STAT3 phosphorylation in non-decidualized and decidualized HESC and enhanced E+MPA-induced decidualization (measured by PRL secretion, P<0.05). LIF mRNA in HESC was down-regulated by decidualization treatment (E+MPA) whereas LIF receptor (R) mRNA was up-regulated, suggesting that the decidualization stimulus 'primed' HESC for LIF action, but that factors not present in our in vitro model were required to induce LIF expression. Ex vivo first trimester decidual biopsies secreted >100 pg/mg G-CSF, IL6, IL8, and MCP1. Decidualized HESC secreted IL6, IL8, IL15 and MCP1. LIF (50 ng/ml) up-regulated IL6 and IL15 (P<0.05) secretion in decidualized HESC compared to 0.5 ng/ml LIF. In murine endometrium, LIF and LIFR immunolocalized to decidualized stromal cells on day 5 of gestation (day 0 = day of plug detection). Western blotting confirmed that LIF and the LIFR were up-regulated in intra-implantation sites compared to inter-implantation sites on Day 5 of gestation. To determine the role of LIF during in vivo murine decidualization, intra-peritoneal injections of a long-acting LIF antagonist (PEGLA; 900 or 1200 µg) were given just post-attachment, during the initiation of decidualization on day 4. PEGLA treatment reduced implantation site decidual area (P<0.05) and desmin staining immuno-intensity (P<0.05) compared to control on day 6 of gestation. This study demonstrated that LIF was an important regulator of decidualization in humans and mice and data provides insight into the processes underlying decidualization, which are important for understanding implantation and placentation.

PMID 21966484

Decidualisation and angiogenesis

Best Pract Res Clin Obstet Gynaecol. 2011 Jun;25(3):259-71. Epub 2010 Dec 8.

Plaisier M. Source Leiden University Medical Centre, PO Box 9600, 2300 RC Leiden, The Netherlands. Margreetp@hotmail.com

Abstract

The timing of decidualisation and vascular processes during the implantation period is of paramount importance for the development of a receptive endometrium suitable for implantation. The endometrium transforms during the secretory phase into a well-vascularised receptive tissue characterised by increased vascular permeability, oedema, proliferation and differentiation of stromal cells into decidual cells, invasion of leucocytes, vascular remodelling and angiogenesis. Decidualisation continues in the presence of conception and an influx of immune cells, trophoblasts and vascular adaptation will occur. Vascular changes include spiral artery remodelling, angiogenesis and the induction of angiogenic factors. Disturbances in uterine blood supply are associated with first-trimester miscarriages and third-trimester perinatal morbidity and mortality caused by pre-eclampsia and foetal growth restriction. This article assesses decidual vascular changes during human implantation, and evaluates the involvement of angiogenesis in the pathogenesis of miscarriages, pre-eclampsia and intrauterine growth restriction.

Copyright © 2010 Elsevier Ltd. All rights reserved.

PMID: 21144801

http://www.ncbi.nlm.nih.gov/pubmed/21144801

SERPINE2, an inhibitor of plasminogen activators, is highly expressed in the human endometrium during the secretory phase

Reprod Biol Endocrinol. 2011 Mar 23;9:38.

Lee RK, Fan CC, Hwu YM, Lu CH, Lin MH, Chen YJ, Li SH. Source Department of Medical Research, Mackay Memorial Hospital, Taipei, Taiwan.

Abstract

BACKGROUND: SERPINE2, also known as protease nexin-1, belongs to the serine protease inhibitor (SERPIN) superfamily. It is one of the potent SERPINs that modulates the activity of plasminogen activators (PAs). PAs and their SERPIN inhibitors, such as SERPINB2 and SERPINE1, were expressed in the human endometrium and were implicated in implantation. However, expression data about SERPINE2 in the human endometrium is still unknown. Thus, we conducted an investigation to reveal the spatiotemporal and cellular expression of SERPINE2 in the human uterus during the menstrual cycle.

METHODS: Seven patients who underwent a hysterectomy and samples of 120 archived patients' endometrial curettage or parts of the uterus that were formalin-fixed and embedded in paraffin. Western blotting was performed to evaluate the specificity and sensitivity of the antibody. Immunohistochemistry was conducted to localize the SERPINE2 expression site. Quantitative analysis was conducted to evaluate expression levels of SERPINE2 in various sub-phases of the menstrual cycle.

RESULTS: The SERPINE2 protein was primarily detected in the uterine fluid during the mid- and late-secretory phases of the menstrual cycle. It was predominantly expressed in the luminal and glandular epithelium, less in the myometrium, and only dispersedly in certain stromal cells throughout the menstrual cycle. A quantitative analysis of expression levels of SERPINE2 in the glandular epithelium revealed that it was highly expressed in the endometrium during the secretory phase compared to the proliferative phase.

CONCLUSIONS: The SERPINE2 protein is highly expressed in the endometrium during the secretory phase, indicating that it may participate in tissue remodeling involved in implantation.

PMID: 21426587

2005

Exp Cell Res. 2005 Feb 1;303(1):101-13. VE-cadherin is a critical molecule for trophoblast-endothelial cell interaction in decidual spiral arteries. Bulla R, Villa A, Bossi F, Cassetti A, Radillo O, Spessotto P, De Seta F, Guaschino S, Tedesco F. Source Department of Physiology and Pathology, University of Trieste, Italy. Abstract Fetal cytotrophoblasts colonize the decidual spiral arteries during pregnancy and partially replace the endothelium by an as yet unknown mechanism. To clarify this issue, we cocultured trophoblast cells (TCs) and decidual endothelial cells (DECs) isolated from first trimester placentae and found by electron microscopic analysis that TCs adhered to DECs and migrated through the interendothelial junctions within 24 h. Since extravillous TCs were shown by FACS analysis to express vascular-endothelial (VE)-cadherin and platelet endothelial cell adhesion molecule-1 (PECAM)-1, we investigated the role of these junctional molecules in TC adhesion to DECs and transendothelial migration of cytotrophoblasts. Both VE-cadherin and PECAM-1 were present at the contact sites between TCs and DECs in decidual sections. TC adhesion and migration were markedly inhibited by mAbs to VE-cadherin and marginally by mAb to PECAM-1. Increased expression of VE-cadherin was observed at the contact areas between TCs and DECs, whereas PECAM-1 was found to be redistributed from intercellular junctions. The induction of apoptosis of DECs by TCs, as the mechanism responsible for their replacement, was ruled out by the negative staining with TUNEL of DECs cocultured with TCs and the absence of DNA fragmentation. In conclusion, VE-cadherin is involved in transendothelial migration of TCs, and replacement of DECs by TCs is not the result of apoptosis.

PMID 15572031