Talk:Placenta - Maternal Decidua: Difference between revisions
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PMID: 21426587 | PMID: 21426587 | ||
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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 | |||
Revision as of 09:51, 21 May 2012
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Cite this page: Hill, M.A. (2024, May 18) Embryology Placenta - Maternal Decidua. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Placenta_-_Maternal_Decidua |
2012
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
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
