Talk:Placenta - Villi Development

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Cite this page: Hill, M.A. (2024, March 29) Embryology Placenta - Villi Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Placenta_-_Villi_Development

2018

Image processing methods for the structural detection and gradation of placental villi

Comput Biol Med. 2018 Sep 1;100:259-269. doi: 10.1016/j.compbiomed.2017.08.004. Epub 2017 Aug 3.

Swiderska-Chadaj Z1, Markiewicz T2, Koktysz R3, Cierniak S4. Author information Abstract The context-based examination of stained tissue specimens is one of the most important procedures in histopathological practice. The development of image processing methods allows for the automation of this process. We propose a method of automatic segmentation of placental structures and assessment of edema present in placental structures from a spontaneous miscarriage. The presented method is based on texture analysis, mathematical morphology, and region growing operations that are applicable to the heterogeneous microscopic images representing histological slides of the placenta. The results presented in this study were obtained using a set of 50 images of single villi originating from 13 histological slides and was compared with the manual evaluation of the pathologist. In the presented experiments, various structures, such as villi, villous mesenchyme, trophoblast, collagen, and vessels have been recognized. Moreover, the gradation of villous edema for three classes (no villous edema, moderate villous edema, and massive villous edema) has been conducted. Villi images were correctly identified in 98.21%, villous mesenchyme was correctly identified in 83.95%, and the villi evaluation was correct in 74% for the edema degree and 86% for the number of vessels. The presented segmentation method may serve as a support for current manual diagnosis methods and reduce the bias related to individual, subjective assessment of experts. KEYWORDS: Histopathology; Image analysis; Image segmentation; Mathematical morphology; Placenta; Texture PMID: 28797713 DOI: 10.1016/j.compbiomed.2017.08.004

2017

Placenta. 2017 Oct;58:52-59. doi: 10.1016/j.placenta.2017.08.005. Epub 2017 Aug 12. Gene markers of normal villous maturation and their expression in placentas with maturational pathology. Leavey K1, Benton SJ2, Grynspan D3, Bainbridge SA4, Morgen EK5, Cox BJ6. Author information Abstract INTRODUCTION: The placenta demonstrates a recognized sequence of histomorphologic maturation throughout pregnancy, and in some cases, shows abnormally advanced (AVM) or delayed (DVM) villous maturation. While AVM and DVM have important clinical implications, it is unknown whether they truly represent a state of accelerated/delayed normal maturation or a state of pathological maldevelopment. The purpose of our study is, therefore, to address this challenge via a genome-wide search for expression markers of normal villous maturation (NM) and the assessment of these genes in cases of maturational pathology. METHODS: A total of 142 placentas, previously evaluated by gene expression microarray, were reviewed histologically and classified as NM, AVM, or DVM. Expression data from healthy NM placentas underwent Pearson correlations with gestational age (GA) and network/pathway analysis to identify candidate gene markers. Candidates were then validated in an independent microarray dataset and used to calculate "molecular GAs" of placentas with maturational pathology. RESULTS: Analysis of NM placentas yielded 17 candidate markers of normal villous maturation, of which 11 were independently validated. Genes with expression increasing across gestation were associated with transcription and metabolism, while those demonstrating decreasing expression were involved in cell cycle and division. Molecular GA was 5.3 weeks older than true GA among AVM placentas (p < 0.001), and 1.1 weeks younger among DVM placentas (p = 0.149). DISCUSSION: We have found evidence of advanced molecular GA in AVM placentas, while molecular alterations in DVM placentas were merely suggestive of delayed maturation. In the future, these findings will need to be validated with additional techniques such as in situ hybridization or immunohistochemistry. Copyright © 2017 Elsevier Ltd. All rights reserved. KEYWORDS: Advanced villous maturity; Delayed villous maturity; Gene signature; Histology; Microarray; Placenta PMID: 28962696 DOI: 10.1016/j.placenta.2017.08.005


2014

Placenta-specific protein 1 (PLAC1) is involved in the trophoblasts invasion and migration

Reproduction. 2014 Jul 2. pii: REP-14-0052. [Epub ahead of print]

Chang W1, Yang Q2, Zhang H3, Lin H4, Zhou Z5, Lu X6, Zhu C7, Xue LQ8, Wang H9.

Abstract

Placenta specific protein 1 (PLAC1), a placenta-specific gene, is implicated in the development of placenta in both humans and mice. However, the precise role of PLAC1 in placental trophoblast function remains unclear. In this study, the localization of PLAC1 in human placental tissues and its physiological significance in trophoblast invasion and migration are investigated by technical studies including real time RT-PCR, in situ hybridization (ISH), immunohistochemistry (IHC), and functional studies by utilizing cell invasion and migration assays in trophoblast cell line HTR8/SVneo as well as the primary inducing extravillous trophoblast cells (EVTs). The results show that PLAC1 is mainly detected in the trophoblast columns (TC) and syncytiotrophoblast (ST) of the first trimester human placental villi, as well as in the EVTs which invade into the maternal decidua. Knockdown of PLAC1 by RNA interference significantly suppresses invasion and migration of HTR8/SVneo cells and shortens the distance of the outgrowth of the induced EVTs from the cytotrophoblast column of the explants. All the above data suggests that PLAC1 plays an important role in human placental trophoblast invasion and migration.

PMID 24989904

Role of IGF2BP3 in trophoblast cell invasion and migration

Cell Death Dis. 2014 Jan 23;5:e1025. doi: 10.1038/cddis.2013.545.

Li W1, Liu D2, Chang W3, Lu X2, Wang YL4, Wang H4, Zhu C4, Lin HY4, Zhang Y5, Zhou J6, Wang H4.

Abstract

The insulin-like growth factor-2 mRNA-binding protein 3 (IGF2BP3) is a member of a highly conserved protein family that is expressed specifically in placenta, testis and various cancers, but is hardly detectable in normal adult tissues. IGF2BP3 has important roles in RNA stabilization and translation, especially during early stages of both human and mouse embryogenesis. Placenta is an indispensable organ in mammalian reproduction that connects developing fetus to the uterine wall, and is responsible for nutrient uptake, waste elimination and gas exchange. Fetus development in the maternal uterine cavity depends on the specialized functional trophoblast. Whether IGF2BP3 plays a role in trophoblast differentiation during placental development has never been examined. The data obtained in this study revealed that IGF2BP3 was highly expressed in human placental villi during early pregnancy, especially in cytotrophoblast cells (CTBs) and trophoblast column, but a much lower level of IGF2BP3 was detected in the third trimester placental villi. Furthermore, the expression level of IGF2BP3 in pre-eclamptic (PE) placentas was significantly lower than the gestational age-matched normal placentas. The role of IGF2BP3 in human trophoblast differentiation was shown by in vitro cell invasion and migration assays and an ex vivo explant culture model. Our data support a role of IGF2BP3 in promoting trophoblast invasion and suggest that abnormal expression of IGF2BP3 might be associated with the etiology of PE.

PMID 24457969

An integrative view on the physiology of human early placental villi

Prog Biophys Mol Biol. 2014 Jan;114(1):33-48. doi: 10.1016/j.pbiomolbio.2013.11.007. Epub 2013 Dec 1.

Huppertz B1, Ghosh D2, Sengupta J3.

Abstract

The placenta is an indispensable organ for intrauterine protection, development and growth of the embryo and fetus. It provides tight contact between mother and conceptus, enabling the exchange of gas, nutrients and waste products. The human placenta is discoidal in shape, and bears a hemo-monochorial interface as well as villous materno-fetal interdigitations. Since Peter Medawar's astonishment to the paradoxical nature of the mother-fetus relationship in 1953, substantial knowledge in the domain of placental physiology has been gathered. In the present essay, an attempt has been made to build an integrated understanding of morphological dynamics, cell biology, and functional aspects of genomic and proteomic expression of human early placental villous trophoblast cells followed by a commentary on the future directions of research in this field. Copyright © 2013 Elsevier Ltd. All rights reserved. KEYWORDS: Early pregnancy loss; IUGR; Placenta; Pre-eclampsia; Transcriptomics; Trophoblast

PMID 24291663

Notch signaling plays a critical role in motility and differentiation of human first-trimester cytotrophoblasts

Endocrinology. 2014 Jan;155(1):263-74. doi: 10.1210/en.2013-1455. Epub 2013 Dec 20.

Haider S1, Meinhardt G, Velicky P, Otti GR, Whitley G, Fiala C, Pollheimer J, Knöfler M.

Abstract

Failures in human extravillous trophoblast (EVT) development could be involved in the pathogenesis of pregnancy diseases. However, the underlying mechanisms have been poorly characterized. Here, we provide evidence that Notch signaling could represent a key regulatory pathway controlling trophoblast proliferation, motility, and differentiation. Immunofluorescence of first-trimester placental tissues revealed expression of Notch receptors (Notch2 and Notch3) and membrane-anchored ligands (delta-like ligand [DLL] 1 and -4 and Jagged [JAG] 1 and -2) in villous cytotrophoblasts (vCTBs), cell column trophoblasts (CCTs), and EVTs. Notch4 and Notch1 were exclusively expressed in vCTBs and in CCTs, respectively. Both proteins decreased in Western blot analyses of first-trimester, primary cytotrophoblasts (CTBs) differentiating on fibronectin. Luciferase reporter analyses suggested basal, canonical Notch activity in SGHPL-5 cells and primary cells that was increased upon seeding on DLL4-coated dishes and diminished in the presence of the Notch/γ-secretase inhibitors N-[N-(3,5-difluorophenacetyl-l-alanyl)]-S-phenylglycine t-butyl ester (DAPT) or L-685,458. Bromodeoxyuridine labeling, cyclin D1 mRNA expression, and cell counting indicated that chemical inhibition of Notch signaling elevated proliferation in the different primary trophoblast model systems. Notch inhibition also increased motility of SGHPL-5 cells through uncoated and fibronectin-coated Transwells, motility of primary CTBs, as well as migration in villous explant cultures on collagen I. Accordingly, small interfering RNA-mediated gene silencing of Notch1 also elevated SGHPL-5 cell migration. In contrast, motility of primary cultures and SGHPL-5 cells was diminished in the presence of DLL4. Moreover, DAPT increased markers of differentiated EVT, ie, human leukocyte antigen G1, integrin α5, and T-cell factor 4, whereas DLL4 provoked the opposite. In summary, the data suggest that canonical Notch signaling impairs motility and differentiation of first-trimester CTBs.

PMID 24189144

2002

Vasculogenesis, angiogenesis and the molecular organisation of endothelial junctions in the early human placenta

J Vasc Res. 2002 May-Jun;39(3):246-59.

Leach L, Babawale MO, Anderson M, Lammiman M. Source School of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Nottingham, Queens Medical Centre, UK. Lopa.Leach@nottingham.ac.uk

Abstract

Vasculogenesis and angiogenesis are regulated by the capacity of endothelial cells to adhere to each other and form new tubes. The presence and role of junctional adhesion molecules during physiological vasculogenesis is unknown. Using ultrastructural and immunocytochemical approaches, we compared the junctional phenotype of developing vessels of the first-trimester human placenta with vessels in the last trimester; the latter include newly formed terminal capillaries and the quiescent vascular bed. First-trimester placental vessels contained the adherens junctional molecules, vascular endothelial cadherin and alpha- and beta-catenin but lacked plakoglobin, the component of fully differentiated adherens junctions. Furthermore, these vessels did not contain the transmembrane tight junctional molecules occludin and claudin-1 and -2. This profile reflects the phenotype of terminal capillaries but differs from large vessels of the full-term placenta. Electron microscopic studies revealed that endothelial tight junctions are present in the first-trimester placenta. Thus, occludin and claudin-1 appear to play no part in the formation of endothelial tight junctions, but are a later requirement. In the early placenta, the predominant growth factor appears to be vascular endothelial growth factor (VEGF), whilst at term, angiopoietin-1 was present in large vessels, with intense angiopoietin-2 immunofluorescence (and VEGF) located in terminal villous capillaries. Thus, endothelial junctions in the human placenta possess two distinct molecular phenotypes, i.e. stable or dynamic, dependent on maturity and plasticity. These distinct phenotypes may be influenced by the angiopoietins/VEGF present in the placenta. Copyright 2002 S. Karger AG, Basel PMID: 12097823