Structural interactions of trophoblast and uterus during hemochorial placenta formation

Enders, Allen C.; Welsh, Alerick O.

doi:10.1002/jez.1402660608

Cited by 77 publications

(58 citation statements)

References 25 publications

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“…A feature of hemochorial placentation found in many species is the movement of trophoblast cells into the uterine parenchyma (Pijnenborg et al, 1981;Enders and Welsh, 1993). These invasive trophoblast cells are epithelial and are guided into the uterine stromal compartment, in large part towards the uterine spiral arteries.…”

Section: Abstract: Trophoblast Invasion Placentation Metrial Glandmentioning

confidence: 99%

A simple in vivo approach to investigate invasive trophoblast cells

Arroyo¹,

Konno²,

Khalili³

et al. 2005

Int. J. Dev. Biol.

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Intrauterine trophoblast cell invasion is an essential part of hemochorial placentation. Aberrant trophoblast cell invasion has been associated with pathologies including preeclampsia and fetal growth restriction. In this study, we describe an in vivo method to assess trophoblast cell invasion using a transgenic rat model, constitutively expressing heat stable human placental alkaline phosphatase (Rosa 26 promoter driven human placental alkaline phosphatase, R26-hAP). Wild-type female Fischer 344 inbred rats were mated with hemizygous R26-hAP transgenic male Fischer 344 rats and sacrificed during the second half of pregnancy. Heat stable alkaline phosphatase (AP) activity associated with the invasive transgenic trophoblast cells was monitored in the wild-type uterine mesometrial compartment and used as an index of trophoblast cell invasion. The expression pattern of cytokeratins by invasive trophoblast cells mimicked the uterine mesometrial distribution of AP activity. Trophoblast cell invasion exhibited a gestation-dependent profile with peak invasion between days 18-20 of pregnancy. In summary, we have devised a simple in vivo method for assessing intrauterine trophoblast cell invasion. This technique should facilitate the discovery of endogenous regulatory mechanisms controlling trophoblast cell invasion and should represent an effective method of testing the impact of various environmental stressors on an essential part of hemochorial placentation. KEY WORDS: trophoblast invasion, placentation, metrial gland, rat pregnancyA feature of hemochorial placentation found in many species is the movement of trophoblast cells into the uterine parenchyma (Pijnenborg et al., 1981;Enders and Welsh, 1993). These invasive trophoblast cells are epithelial and are guided into the uterine stromal compartment, in large part towards the uterine spiral arteries. During pregnancy uterine spiral arteries are modified, increasing the capacity of blood flow to the fetus and allowing maternal blood to directly bathe trophoblast cells; facilitating nutrient and waste exchange. Invasive trophoblast cells are hypothesized to participate in the pregnancy-dependent uterine vascular remodeling (Kam et al., 1999; Nanev et al., 2000). Abnormalities in trophoblast invasion are a prominent feature of diseases of pregnancy, including those associated with preeclampsia, intrauterine growth restriction and anemias (Brosens et al., 2002;Kaufmann et al., 2003). Invasive trophoblast cells represent a specialized trophoblast lineage. The course of their development and functions are poorly understood, as are the regulatory factors in the uteroplacental milieu that guide their Int. J. Dev. Biol. 49: 977-980 (2005) doi: 10.1387/ijdb.051993ja passage. Most investigative work on trophoblast invasion has utilized trophoblast recovered from human pregnancies and consequently has been largely descriptive. Availability of an experimental animal model could be a useful tool in elucidating the biology of invasive trophoblast cells.The invasive tro...

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Section: Abstract: Trophoblast Invasion Placentation Metrial Glandmentioning

confidence: 99%

A simple in vivo approach to investigate invasive trophoblast cells

Arroyo¹,

Konno²,

Khalili³

et al. 2005

Int. J. Dev. Biol.

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“…Hemochorial placentation, which occurs in both primates and rodents, results in the establishment of a close connection between maternal and fetal tissues (Enders and Welsh, 1993;Carson et al, 2000). This close connection facilitates the exchange of nutrients and wastes.…”

Section: Introductionmentioning

confidence: 99%

A uterine decidual cell cytokine ensures pregnancy-dependent adaptations to a physiological stressor

et al. 2007

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In the mouse, decidual cells differentiate from uterine stromal cells in response to steroid hormones and signals arising from the embryo. Decidual cells are crucially involved in creating the intrauterine environment conducive to embryonic development. Among their many functions is the production of cytokines related to prolactin (PRL), including decidual prolactin-related protein (DPRP). DPRP is a heparin-binding cytokine, which is abundantly expressed in uterine decidua. In this investigation, we have isolated the mouse Dprp gene, characterized its structure and evaluated its biological role. Dprp-null mice were made by replacing exons 2 to 6 of the Dprp gene with an in-frame enhanced green fluorescent protein (EGFP) gene and a neomycin (neo) resistance cassette. Heterozygous intercross breeding of the mutant mice yielded the expected mendelian ratio. Pregnant heterozygote females expressed EGFP within decidual tissue in locations identical to endogenous Dprp mRNA and protein expression. Homozygous Dprpnull mutant male and female mice were viable, exhibited normal postnatal growth rates, were fertile and produced normal litter sizes. A prominent phenotype was observed when pregnant Dprp-null mice were exposed to a physiological stressor. DPRP deficiency interfered with pregnancy-dependent adaptations to hypoxia resulting in pregnancy failure. Termination of pregnancy was associated with aberrations in mesometrial decidual cells, mesometrial vascular integrity, and disruptions in chorioallantoic placenta morphogenesis. The observations suggest that DPRP participates in pregnancy-dependent adaptations to a physiological stressor.

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“…They are specialized, exhibit distinct phenotypes, and arise via a multilineage differentiation process (Gardner and Beddington, 1988). Trophoblast lineages go on to contribute to the formation of the chorioallantoic placenta (Enders and Welsh, 1993). These structures are responsible for controlling fetal and maternal environments during pregnancy.…”

Section: Sources Of Pregnancy-specific Modulatorsmentioning

confidence: 99%

Characteristics of the Fetal/Maternal Interface with Potential Usefulness in the Development of Future Immunological and Pharmacological Strategies

Audus

Soares²,

Hunt³

2002

J Pharmacol Exp Ther

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A study of the fundamental biology of the maternal-fetal interface reveals the complex interactions among multiple cell types and regulatory factors necessary to support a successful pregnancy. Cells of decidua and trophoblast lineages play central roles in creating the maternal-fetal interface and are sources of regulatory factors that can determine the quality and success of pregnancy. The regulatory factors considered here are major placental histocompatibility complex proteins, pregnancy-specific regulatory factors for uterine inflammatory cells, and hormone-controlled placental multidrug-resistant transport systems. Potential targets are discussed and presented as areas where researchers may identify novel pharmacological and immunological strategies that eventually will extend to the clinic to improve the quality and success of pregnancy.The milieu comprising the complex maternal-fetal interface is normally a precisely choreographed interplay among multiple cell types and regulatory factors that results in the immunologically safe and nurturing surroundings required to support growth and development of the embryo and fetus. Generally, two cell lineages, decidua and trophoblast, are involved in both secretion of and responses to several regulatory factors that modify the maternal-fetal interface surroundings to create the necessary conditions and anatomical structures to protect the mother and the fetus. The regulatory factors include chemokines, cytokines, growth factors, antigens, and hormones. On occasion, cell secretions of regulatory factors or responsiveness to these regulatory factors are disrupted with the ultimate consequences being pregnancy termination, or intrauterine growth retardation, or potentially maternal compromise. As a consequence, characterization of the fundamental biology of the maternal-fetal interface should expose new targets for therapeutic interventions appropriate to protect mother and fetus.This perspective considers the roles of decidual and trophoblast cells as sources of major placental histocompatibility complex proteins and their influence on maternal inflammatory and immune cell responses, pregnancy-specific regulatory factors for uterine inflammatory cells, and hormoneregulated placental multidrug-resistant transport systems. Although representing three distinct areas, each represents a major player as a protective mechanism for the mother and the fetus. It is clear, for example, that human leukocyte antigens (HLAs) and pregnancy-specific regulatory factors enable the maternal immune system to change and cope with pregnancy and protect the fetal-maternal interface from immune disorders. Based on an understanding of these functions, interventions might someday be developed that enable mothers prone to immune disorders to avoid conditions reThe studies in the laboratory of Dr.

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Structural interactions of trophoblast and uterus during hemochorial placenta formation

Cited by 77 publications

References 25 publications

A simple in vivo approach to investigate invasive trophoblast cells

A simple in vivo approach to investigate invasive trophoblast cells

A uterine decidual cell cytokine ensures pregnancy-dependent adaptations to a physiological stressor

Characteristics of the Fetal/Maternal Interface with Potential Usefulness in the Development of Future Immunological and Pharmacological Strategies

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