Growth characteristics of diabetic rat ectoplacental cones in vivo and in vitro

Caluwaerts, Silvia; Pijnenborg, Robert; Luyten, C; Assche, F.A. Van

doi:10.1007/s001250051473

Cited by 14 publications

(7 citation statements)

References 29 publications

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“…Recent experiments have also shown that exposing mouse ectoplacental cone cells to high d-glucose stimulated these explants into excessive outgrowth [24]. In addition, abnormally high numbers of giant trophoblasts have been observed in utero-placental units of diabetic rats [25, R. Lea and S. Pampfer, unpublished data].…”

Section: Discussionmentioning

confidence: 98%

Decreased expression of fibroblast growth factor-4 and associated dysregulation of trophoblast differentiation in mouse blastocysts exposed to high D-glucose in vitro

2001

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Shortly before becoming involved in the process of implantation into the uterine wall, mammalian embryos reach the blastocyst stage. Two distinct cell lineages, the trophectoderm (TE) and the inner cell mass (ICM) are already present in these embryos.The peripheral TE consists of a single layer of epithelioid cells that differentiates into trophoblasts and contributes to the formation of the placenta. The ICM, in contrast, is an inner cluster of totipotent stem cells that continue to diversify into a variety of cell types to generate the different fetal tissues and organs during organogenesis. Studies have shown that ICM cells and TE cells have many different cellular, biochemical and molecular characteristics, including their susceptibility to embryotoxic agents [1].Pre-conceptional maternal diabetes could already induce subtle cellular, biochemical and molecular damage in the embryos during the blastocyst period. These deficiencies are thought to predispose the em- Abstract Aims/hypothesis. Paracrine interactions are thought to operate between the inner cell mass and trophectoderm cell lineages to co-ordinate their expansion and differentiation during embryo implantation. We aimed to determine whether hyperglycaemia could interfere with this regulatory process. Methods. Mouse blastocysts were pre-exposed to either control or high concentrations of d-glucose for 24 h in vitro and tested for their ability to attach and spread over a fibronectin-coated culture substrate. Quantitative immunocytochemistry was done on blastocysts to assess the protein expression of Fibroblast Growth Factor-4, a growth factor preferentially produced by the inner cell mass and thought to restrict trophectoderm differentiation into giant trophoblasts. Experiments were then done combining the pre-exposure to high d-glucose with the addition of recombinant fibroblast growth factor-4.Results. Compared with control blastocysts, high dglucose pre-treated embryos were found to form 18 % larger trophoblast outgrowths. These blastocysts also showed a 30 % reduction in the expression of fibroblast growth factor-4 protein by inner cell mass cells as they were outgrowing. The trophoblast surface area per outgrowth and the trophoblast nuclear area were corrected when the addition of recombinant fibroblast growth factor-4 was combined with the pre-exposure to high d-glucose. Conclusion/interpretation. The data suggests that trophectoderm differentiation is impaired by high d-glucose and that this effect is secondary to a deficiency in fibroblast growth factor-4 protein in the inner cell mass. These observations add a novel perspective to the study of the peri-implantation embryopathy associated with maternal diabetes. [Diabetologia (2001

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Section: Discussionmentioning

confidence: 98%

Decreased expression of fibroblast growth factor-4 and associated dysregulation of trophoblast differentiation in mouse blastocysts exposed to high D-glucose in vitro

2001

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“…However, decreased LI was observed in the placenta of adolescent overnourished ewes during mid to late gestation, which were also characterized by impaired fetal and placental growth [56,57]. Moreover, in pregnancies compromised by diabetes, both increased and decreased placental cell proliferation was observed in rats [58,59]. For diabetic mice, decreased cell proliferation was reported in the myometrium during early pregnancy [60].…”

Section: Discussionmentioning

confidence: 99%

Placental development during early pregnancy in sheep: Effects of embryo origin on fetal and placental growth and global methylation

et al. 2013

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The origin of embryos including those created through assisted reproductive technologies (ART) may have profound effects on placental and fetal development, possibly leading to compromised pregnancies associated with poor placental development. To determine the effects of embryo origin on fetal size, and maternal and fetal placental cellular proliferation and global methylation, pregnancies were achieved through natural mating (NAT), or transfer of embryos generated through in vivo (NAT-ET), IVF, or in vitro activation (IVA). On Day 22 of pregnancy, fetuses were measured and placental tissues were collected to immunodetect Ki67 (a marker of proliferating cells) and 5-methyl cytosine (5mC) followed by image analysis, and determination of mRNA expression for three DNA methyltransferases (DNMT). Fetal length and labeling index (proportion of proliferating cells) in maternal caruncles (CAR; maternal placenta) and fetal membranes (FM; fetal placenta) were less (P < 0.001) in NAT-ET, IVF and IVA than in NAT. Expression of 5mC was greater (P < 0.02) in IVF and IVA than in NAT. In CAR, mRNA expression for DNMT1 was greater (P < 0.01) in IVA compared to the other groups, but DNMT3A expression was less (P < 0.04) in NAT-ET and IVA than NAT. In FM, expression of mRNA for DNMT3A was greater (P < 0.01) in IVA compared to the other groups, and was similar in NAT, NAT-ET and IVF groups. Thus, embryo origin may have specific effects on growth and function of ovine utero-placental and fetal tissues through regulation of tissue growth, DNA methylation and likely other mechanisms. These data provide a foundation for determining expression of specific factors regulating placental and fetal tissue growth and function in normal and compromised pregnancies, including those achieved with ART.

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“…Ectoplacental cones from diabetic rats are reduced in mitotic index and in vitro outgrowth [56]. Ectoplacental cones from diabetic rats are reduced in mitotic index and in vitro outgrowth [56].…”

Section: Pro-inflammatory Agent Referencementioning

confidence: 98%

Diabetic Pregnancies: The Challenge of Developing in a Pro-Inflammatory Environment

Jawerbaum

González²

2006

CMC

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The maternal diabetic environment alters the embryo and the feto-placental development. The results of these alterations are: increased embryo resorption and malformation rates, placental dysfunction, fetal alterations that lead to increased neonatal morbidity and mortality rates, and also diseases that will be evident later in the adult life of the newborn. The etiology of these many maternal diabetes-induced complications are not yet understood in full. In this review the role of maternal diabetes as an inductor of a pro-inflammatory environment that impairs embryo and placental development is discussed. An overproduction of pro-inflammatory agents is found in the uterus during implantation and the developing embryo and placenta from experimental models of diabetes, as well as in placenta from diabetic women. In these tissues there are increases in reactive oxygen species, pro-inflammatory cytokines and prostaglandins, nitric oxide and peroxynitrites. These pro-inflammatory agents lead to the intrauterine activation of matrix metalloproteinases, proteases involved in remodeling the extracellular matrix during implantation and feto-placental development. Many of these pro-inflammatory agents have overlapping mechanisms of action and cross regulatory pathways that propagate the inflammatory processes. Antioxidants, PPARgamma activators, and NF-kappaB inhibitors are able to reduce the concentrations of these agents in intrauterine gestational tissues. This article reviews the current understanding of maternal diabetes-induced changes in pro-inflammatory and anti-inflammatory pathways that affect the embryo and placental development in maternal diabetes, and stresses the need of a strict maternal control of the pathology to prevent deleterious consequences in the offspring.

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Growth characteristics of diabetic rat ectoplacental cones in vivo and in vitro

Cited by 14 publications

References 29 publications

Decreased expression of fibroblast growth factor-4 and associated dysregulation of trophoblast differentiation in mouse blastocysts exposed to high D-glucose in vitro

Decreased expression of fibroblast growth factor-4 and associated dysregulation of trophoblast differentiation in mouse blastocysts exposed to high D-glucose in vitro

Placental development during early pregnancy in sheep: Effects of embryo origin on fetal and placental growth and global methylation

Diabetic Pregnancies: The Challenge of Developing in a Pro-Inflammatory Environment

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