The rat possesses hemochorial placentation with deep intrauterine trophoblast cell invasion and trophoblast-directed uterine spiral artery remodeling; features shared with human placentation. Recognition of these similarities spurred the establishment of in vitro and in vivo research methods using the rat as an animal model to address mechanistic questions regarding development of the hemochorial placenta. The purpose of this review is to provide the requisite background to help move the rat to the forefront in placentation research.
PMID: 22284666 [PubMed - as supplied by publisher]
Placenta accreta: Pathogenesis of a 20th century iatrogenic uterine disease.
Placenta. 2012 Jan 25;
Authors: Jauniaux E, Jurkovic D
Abstract
Placenta accreta refers to different grades of abnormal placental attachment to the uterine wall, which are characterised by invasion of trophoblast into the myometrium. Placenta accreta has only been described and studied by pathologists for less than a century. The fact that the first detailed description of a placenta accreta happened within a couple of decades of major changes in the caesarean surgical techniques is highly suggestive of a direct relationship between prior uterine surgery and abnormal placenta adherence. Several concepts have been proposed to explain the abnormal placentation in placenta accreta including a primary defect of the trophoblast function, a secondary basalis defect due to a failure of normal decidualization and more recently an abnormal vascularisation and tissue oxygenation of the scar area. The vast majority of placenta accreta are found in women presenting with a previous history of caesarean section and a placenta praevia. Recent epidemiological studies have also found that the strongest risk factor for placenta praevia is a prior caesarean section suggesting that a failure of decidualization in the area of a previous uterine scar can have an impact on both implantation and placentation. Ultrasound studies of uterine caesarean section scar have shown that large and deep myometrial defects are often associated with absence of re-epithelialisation of the scar area. These findings support the concept of a primary deciduo-myometrium defect in placenta accreta, exposing the myometrium and its vasculature below the junctional zone to the migrating trophoblast. The loss of this normal plane of cleavage and the excessive vascular remodelling of the radial and arcuate arteries can explain the in-vivo findings and the clinical consequence of placenta accreta. Overall these data support the concept that abnormal decidualization and trophoblastic changes of the placental bed in placenta accreta are secondary to the uterine scar and thus entirely iatrogenic.
PMID: 22284667 [PubMed - as supplied by publisher]
Review: Placental perturbations induce the developmental abnormalities often observed in bovine somatic cell nuclear transfer.
Placenta. 2012 Feb;33 Suppl:S99-S104
Authors: Chavatte-Palmer P, Camous S, Jammes H, Le Cleac’h N, Guillomot M, Lee RS
Abstract
Since the first success in cloning sheep, the production of viable animals by somatic cell nuclear transfer (SCNT) has developed significantly. Cattle are by far the most successfully cloned species but, despite this, the technique is still associated with a high incidence of pregnancy failure and accompanying placental and fetal pathologies. Pre- and early post-implantation losses can affect up to 70% of the pregnancies. In the surviving pregnancies, placentomegaly and fetal overgrowth are commonly observed, but the incidence varies widely, depending on the genotype of the nuclear donor cell and differences in SCNT procedures. In all cases, the placenta is central to the onset of the pathologies. Although cellular organisation of the SCNT placenta appears normal, placental vascularisation is modified and fetal-to-maternal tissue ratios are slightly increased in the SCNT placentomes. In terms of functionality, steroidogenesis is perturbed and abnormal estrogen production and metabolism probably play an important part in the increased gestation length and lack of preparation for parturition observed in SCNT recipients. Maternal plasma concentrations of pregnancy-associated glycoproteins are increased, mostly due to a reduction in turnover rate rather than increased placental production. Placental glucose transport and fructose synthesis appear to be modified and hyperfructosemia has been observed in neonatal SCNT calves. Gene expression analyses of the bovine SCNT placenta show that multiple pathways and functions are affected. Abnormal epigenetic re-programming appears to be a key component of the observed pathologies, as shown by studies on the expression of imprinted genes in SCNT placenta.
IFPA Award in Placentology Lecture: Molecular regulation of human trophoblast invasion.
Placenta. 2012 Feb;33 Suppl:S55-62
Authors: Knöfler M, Pollheimer J
Abstract
Invasion of extravillous trophoblast cell types into maternal uterine tissues is essential for successful human placental development and progression of pregnancy. Whereas endovascular trophoblasts migrate into the maternal spiral arteries, interstitial trophoblasts invade the decidual stroma, colonize the vessels from outside and communicate with diverse uterine cell types such as decidual stromal cells, macrophages and uterine NK cells. For example, interstitial trophoblasts expressing polymorphic human leukocyte antigen-C interact with uterine NK cells through binding to their killer immunoglobulin-like receptors which likely plays a role in trophoblast invasion and reproductive success of pregnancy. Both extravillous trophoblast subtypes are critically involved in the vascular transformation of the spiral arteries into dilated conduits ensuring appropriate blood flow into the intervillous space. Failures in this remodeling process are thought to be associated with severe forms of fetal growth restriction, preeclampsia and other pregnancy complications warranting studies on the molecular regulation of extravillous trophoblast differentiation. Moreover, interstitial trophoblast-derived hormones may regulate diverse biological functions in the decidua. In particular, human chorionic gonadotrophin has been shown to promote angiogenesis and to suppress apoptosis of endometrial stromal cells. In return, decidual cells produce a plethora of soluble factors controlling trophoblast invasion in a time- and distance-dependent manner. However, the underlying mechanisms have not been fully elucidated. Here, we will summarize autocrine as well as paracrine factors regulating invasion of extravillous trophoblasts and discuss critical signaling cascades involved. In addition, we will focus on key regulatory transcription factors controlling cell column proliferation and differentiation of the human extravillous trophoblast.
Review: The evolving placenta: Different developmental paths to a hemochorial relationship.
Placenta. 2012 Feb;33 Suppl:S92-8
Authors: Enders AC, Carter AM
Abstract
The way in which maternal blood is associated with trophoblast prior to the formation of the different types of hemochorial placenta may be conveniently grouped into four main patterns: a transitory endotheliochorial condition; maternal blood released into a mass of trophoblast; maternal blood confined to lacunae; and fetal villi entering preexisting maternal blood sinuses. Although it might be considered logical that developing placentas would pass through an endotheliochorial stage to become hemochorial, this developmental pattern is seen only as a transient stage in several species of bats and sciuromorph rodents. More commonly a mass of trophoblast at the junction with the endometrium serves as a meshwork through which maternal blood passes, with subsequent organization of a labyrinth when the fetal vascular component is organized. The initial trophoblast meshwork may be cellular or syncytial, often leading to a similar relationship in the spongy zone and labyrinth. Old World monkeys, apes and humans have a lacunar stage prior to establishing a villous hemochorial condition. New World monkeys lack a true lacunar stage, retaining portions of maternal vessels for some time and initially forming a trabecular arrangement similar to though differently arrived at than that in the tarsier. In armadillos, preexisting maternal venous sinuses are converted into an intervillous blood space by intruding fetal villi. Variations from the major patterns of development also occur. The way in which the definitive placental form is achieved developmentally should be considered when using placental structure to extrapolate evolution of placentation.
Review: The feto-placental unit, pregnancy pathology and impact on long term maternal health.
Placenta. 2012 Feb;33 Suppl:S37-41
Authors: Clifton VL, Stark MJ, Osei-Kumah A, Hodyl NA
Abstract
Pregnancy induces a number of alterations to maternal physiology to accommodate the increased demands made by the developing fetus and placenta. These alterations appear at least in part to be driven by products derived from the feto-placental unit, including microchimeric cells, as well as placental exosomes and microparticles, inducing changes to maternal physiology both during pregnancy and beyond. Further, increasing evidence suggests that some of these alterations are dependent on the sex of the fetus. Pre-eclampsia and asthma represent two common pregnancy complications that have provided valuable insight into how the feto-placental unit influences maternal physiology in a sex-specific manner. Pregnancy-induced alterations in maternal physiology may expose pre-existing subclinical pathologies and provide insight into future maternal health and disease. While most pregnancy-induced alterations to the maternal system are reversed following delivery, some can persist after parturition leading to cardiovascular, metabolic and autoimmune disease and increased risk of early mortality.
Review: Spatiotemporal dynamics of hCG/cAMP signaling and regulation of placental function.
Placenta. 2012 Feb;33 Suppl:S87-91
Authors: Weedon-Fekjær MS, Taskén K
Abstract
The pregnancy hormone human chorionic gonadotropin (hCG) is essential to sustain early pregnancy and involved in regulation of progesterone production, decidualization, and cytotrophoblast differentiation. It binds to and activates the G-protein coupled luteinizing hormone/hCG-receptor, activating the cAMP/protein kinase A (PKA) pathway which results in the phosphorylation of specific intracellular target proteins. Specificity in cAMP signaling is ensured by generation of localized pools of cAMP controlled by phosphodiesterases and by discrete spatial and temporal activation of PKA in supramolecular signaling clusters inside the cell organized by A-kinase-anchoring proteins. Here we discuss spatiotemporal regulation of PKA signaling in response to hCG controlling placental function.
Review: Human trophoblast fusion and differentiation: Lessons from trisomy 21 placenta.
Placenta. 2012 Feb;33 Suppl:S81-6
Authors: Pidoux G, Gerbaud P, Cocquebert M, Segond N, Badet J, Fournier T, Guibourdenche J, Evain-Brion D
Abstract
The syncytiotrophoblast layer plays a major role throughout pregnancy, since it is the site of numerous placental functions, including ion and nutrient exchange and the synthesis of steroid and peptide hormones required for fetal growth and development. Inadequate formation and regeneration of this tissue contributes to several pathologies of pregnancy such as intrauterine growth restriction and preeclampsia, which may lead to iatrogenic preterm delivery in order to prevent fetal death and maternal complications. Syncytiotrophoblast formation can be reproduced in vitro using different models. For the last ten years we have routinely purified villous cytotrophoblastic cells (CT) from normal first, second and third trimester placentas and from gestational age-matched Trisomy 21 placentas. We cultured villous CT on plastic dishes to follow the molecular and biochemical aspects of their morphological and functional differentiation. Taking advantage of this unique collection of samples, we here discuss the concept that trophoblast fusion and functional differentiation may be two differentially regulated processes, which are linked but quite distinct. We highlight the major role of mesenchymal-trophoblast cross talk in regulating trophoblast cell fusion. We suggest that the oxidative status of the trophoblast may regulate glycosylation of proteins, including hCG, and thereby modulate major trophoblast cell functions.
PMID: 22138060 [PubMed - in process]
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