Identification of two new nonclassical members of the rat prolactin family

2000 ◽  
Vol 24 (1) ◽  
pp. 95-108 ◽  
Author(s):  
N Sahgal ◽  
GT Knipp ◽  
B Liu ◽  
BM Chapman ◽  
G Dai ◽  
...  
Keyword(s):  
Giant Cell ◽  
Cell Layer ◽  
Giant Cells ◽  
Trophoblast Giant Cell ◽  
Related Protein ◽  
Junctional Zone ◽  
Dbest Database ◽  
Chorioallantoic Placenta ◽  
Trophoblast Giant Cells ◽  
Ectoplacental Cone

The prolactin (PRL) family is comprised of a group of hormones/cytokines that are expressed in the anterior pituitary, uterus, and placenta. These proteins participate in the control of maternal and fetal adaptations to pregnancy. In this report, we have identified two new nonclassical members of the rat PRL family through a search of the National Center for Biotechnology Information dbEST database. The cDNAs were sequenced and their corresponding mRNAs characterized. Overall, the rat cDNAs showed considerable structural similarities with mouse proliferin-related protein (PLF-RP) and prolactin-like protein-F (PLP-F), consistent with their classification as rat homologs for PLF-RP and PLP-F. The expression of both cytokines/hormones was restricted to the placenta. The intraplacental sites of PLF-RP and PLP-F synthesis differed in the rat and the mouse. In the mouse, PLF-RP was expressed in the trophoblast giant cell layer of the midgestation chorioallantoic and choriovitelline placentas and, during later gestation, in the trophoblast giant cell and spongiotrophoblast layers within the junctional zone of the mouse chorioallantoic placenta. In contrast, in the rat, PLF-RP was first expressed in the primordium of the chorioallantoic placenta (ectoplacental cone region) and, later, exclusively within the labyrinth zone of the chorioallantoic placenta. In the mouse, PLP-F is an exclusive product of the spongiotrophoblast layer, whereas in the rat, trophoblast giant cells were found to be the major source of PLP-F, with a lesser contribution from spongiotrophoblast cells late in gestation. In summary, we have established the presence of PLF-RP and PLP-F in the rat.

scholarly journals Keratin 8 protection of placental barrier function

2003 ◽  
Vol 161 (4) ◽  
pp. 749-756 ◽  
Author(s):  
Daniel Jaquemar ◽  
Sergey Kupriyanov ◽  
Miriam Wankell ◽  
Jacqueline Avis ◽  
Kurt Benirschke ◽  
...  
Keyword(s):  
Giant Cell ◽  
Barrier Function ◽  
Genetic Background ◽  
Cell Layer ◽  
Giant Cells ◽  
Intermediate Filament Protein ◽  
Trophoblast Giant Cell ◽  
Primary Defect ◽  
Keratin 8 ◽  
Filament Protein

The intermediate filament protein keratin 8 (K8) is critical for the development of most mouse embryos beyond midgestation. We find that 68% of K8−/− embryos, in a sensitive genetic background, are rescued from placental bleeding and subsequent death by cellular complementation with wild-type tetraploid extraembryonic cells. This indicates that the primary defect responsible for K8−/− lethality is trophoblast giant cell layer failure. Furthermore, the genetic absence of maternal but not paternal TNF doubles the number of viable K8−/− embryos. Finally, we show that K8−/− concepti are more sensitive to a TNF-dependent epithelial apoptosis induced by the administration of concanavalin A (ConA) to pregnant mothers. The ConA-induced failure of the trophoblast giant cell barrier results in hematoma formation between the trophoblast giant cell layer and the embryonic yolk sac in a phenocopy of dying K8-deficient concepti in a sensitive genetic background. We conclude the lethality of K8−/− embryos is due to a TNF-sensitive failure of trophoblast giant cell barrier function. The keratin-dependent protection of trophoblast giant cells from a maternal TNF-dependent apoptotic challenge may be a key function of simple epithelial keratins.

The mechanism of mouse egg-cylinder morphogenesis in vitro

Development ◽  
1981 ◽  
Vol 61 (1) ◽  
pp. 277-287
Author(s):  
A. J. Copp
Keyword(s):  
Giant Cell ◽  
Cell Formation ◽  
Cell Movement ◽  
Giant Cells ◽  
Cell Number ◽  
Dependent Change ◽  
Morphogenesis In Vitro ◽  
Trophoblast Giant Cells

The number of trophoblast giant cells in outgrowths of mouse blastocysts was determined before, during and after egg-cylinder formation in vitro. Giant-cell numbers rose initially but reached a plateau 12 h before the egg cylinder appeared. A secondary increase began 24 h after egg-cylinder formation. Blastocysts whose mural trophectoderm cells were removed before or shortly after attachment in vitro formed egg cylinders at the same time as intact blastocysts but their trophoblast outgrowths contained fewer giant cells at this time. The results support the idea that egg-cylinder formation in vitro is accompanied by a redirection of the polar to mural trophectoderm cell movement which characterizes blastocysts before implantation. The resumption of giant-cell number increase in trophoblast outgrowths after egg-cylinder formation may correspond to secondary giant-cell formation in vivo. It is suggested that a time-dependent change in the strength of trophoblast cell adhesion to the substratum occurs after blastocyst attachment in vitro which restricts the further entry of polar cells into the outgrowth and therefore results in egg-cylinder formation.

Abstract 3542: Abnormal intracytoplasmic accumulation of autophagy-related protein p62/SQSTM1 characterizes giant cells of giant cell tumor of bone

2016 ◽  
Author(s):  
Toru Motoi ◽  
Akihiko Yoshida ◽  
Noriko Motoi ◽  
Ikuma Kato ◽  
Tomotake Okuma ◽  
...  
Keyword(s):  
Giant Cell Tumor ◽  
Giant Cell ◽  
Giant Cells ◽  
Cell Tumor ◽  
Related Protein

In vivo and in vitro development of mouse embryos homozygous for the embryonic lethal velvet coat (Ve) mutation

Development ◽  
1981 ◽  
Vol 66 (1) ◽  
pp. 43-55
Author(s):  
J. Rossant ◽  
K. M. Vijh
Keyword(s):  
Inner Cell Mass ◽  
Cell Mass ◽  
Giant Cells ◽  
Blastocyst Stage ◽  
Parietal Endoderm ◽  
Trophoblast Giant Cells ◽  
Vitro Development ◽  
Ectoplacental Cone

Embryos homozygous for the velvet coat mutation, Ve/Ve, were recognized at 6·5 days post coitum by the reduced size of the ectodermal portions of the egg cylinder and the loose, columnar nature of the overlying endoderm. Later in development ectoderm tissues were sometimes entirely absent. Abnormalities appeared in the ectoplacental cone at 8·5 days but trophoblast giant cells and parietal endoderm appeared unaffected. Homozygotes could not be unequivocally identified at 5·5 days nor at the blastocyst stage but were recognized in blastocyst outgrowths by poor development of the inner cell mass derivatives, It has previously been suggested that Ve may exert its action at the blastocyst stage by reducing the size of the inner cell mass, but no evidence for such a reduction was found. Most of the observations on Ve/Ve homozygotes are, however, consistent with the hypothesis that Ve exerts its action primarily on later primitive ectoderm development.

scholarly journals Differentiation of Trophoblast Giant Cells and Their Metabolic Functions Are Dependent on Peroxisome Proliferator-Activated Receptor β/δ

2006 ◽  
Vol 26 (8) ◽  
pp. 3266-3281 ◽  
Author(s):  
Karim Nadra ◽  
Silvia I. Anghel ◽  
Elisabeth Joye ◽  
Nguan Soon Tan ◽  
Sharmila Basu-Modak ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Giant Cell ◽  
Giant Cells ◽  
Peroxisome Proliferator ◽  
Phosphatidylinositol 3 Kinase ◽  
Peroxisome Proliferator Activated Receptor ◽  
Metabolic Functions ◽  
Integrin Linked Kinase ◽  
Trophoblast Giant Cells

ABSTRACT Mutation of the nuclear receptor peroxisome proliferator-activated receptor β/δ (PPARβ/δ) severely affects placenta development, leading to embryonic death at embryonic day 9.5 (E9.5) to E10.5 of most, but not all, PPARβ/δ-null mutant embryos. While very little is known at present about the pathway governed by PPARβ/δ in the developing placenta, this paper demonstrates that the main alteration of the placenta of PPARβ/δ-null embryos is found in the giant cell layer. PPARβ/δ activity is in fact essential for the differentiation of the Rcho-1 cells in giant cells, as shown by the severe inhibition of differentiation once PPARβ/δ is silenced. Conversely, exposure of Rcho-1 cells to a PPARβ/δ agonist triggers a massive differentiation via increased expression of 3-phosphoinositide-dependent kinase 1 and integrin-linked kinase and subsequent phosphorylation of Akt. The links between PPARβ/δ activity in giant cells and its role on Akt activity are further strengthened by the remarkable pattern of phospho-Akt expression in vivo at E9.5, specifically in the nucleus of the giant cells. In addition to this phosphatidylinositol 3-kinase/Akt main pathway, PPARβ/δ also induced giant cell differentiation via increased expression of I-mfa, an inhibitor of Mash-2 activity. Finally, giant cell differentiation at E9.5 is accompanied by a PPARβ/δ-dependent accumulation of lipid droplets and an increased expression of the adipose differentiation-related protein (also called adipophilin), which may participate to lipid metabolism and/or steroidogenesis. Altogether, this important role of PPARβ/δ in placenta development and giant cell differentiation should be considered when contemplating the potency of PPARβ/δ agonist as therapeutic agents of broad application.

scholarly journals The HAND1 Basic Helix-Loop-Helix Transcription Factor Regulates Trophoblast Differentiation via Multiple Mechanisms

2000 ◽  
Vol 20 (2) ◽  
pp. 530-541 ◽  
Author(s):  
Ian C. Scott ◽  
Lynn Anson-Cartwright ◽  
Paul Riley ◽  
Danny Reda ◽  
James C. Cross
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Giant Cell ◽  
Giant Cells ◽  
Mutant Phenotype ◽  
Bhlh Transcription Factor ◽  
Placental Development ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix ◽  
Ectoplacental Cone

ABSTRACT The basic helix-loop-helix (bHLH) transcription factor genesHand1 and Mash2 are essential for placental development in mice. Hand1 promotes differentiation of trophoblast giant cells, whereas Mash2 is required for the maintenance of giant cell precursors, and its overexpression prevents giant cell differentiation. We found that Hand1 expression and Mash2 expression overlap in the ectoplacental cone and spongiotrophoblast, layers of the placenta that contain the giant cell precursors, indicating that the antagonistic activities ofHand1 and Mash2 must be coordinated. MASH2 and HAND1 both heterodimerize with E factors, bHLH proteins that are the DNA-binding partners for most class B bHLH factors and which are also expressed in the ectoplacental cone and spongiotrophoblast. In vitro, HAND1 could antagonize MASH2 function by competing for E-factor binding. However, the Hand1 mutant phenotype cannot be solely explained by ectopic activity of MASH2, as the Hand1mutant phenotype was not altered by further mutation ofMash2. Interestingly, expression of E-factor genes (ITF2 and ALF1) was down-regulated in the trophoblast lineage prior to giant cell differentiation. Therefore, suppression of MASH2 function, required to allow giant cell differentiation, may occur in vivo by loss of its E-factor partner due to loss of its expression and/or competition from HAND1. In giant cells, where E-factor expression was not detected, HAND1 presumably associates with a different bHLH partner. This may account for the distinct functions of HAND1 in giant cells and their precursors. We conclude that development of the trophoblast lineage is regulated by the interacting functions of HAND1, MASH2, and their cofactors.

Properties of extra-embryonic ectoderm isolated from postimplantation mouse embryos

Development ◽  
1977 ◽  
Vol 39 (1) ◽  
pp. 183-194
Author(s):  
J. Rossant ◽  
L. Ofer
Keyword(s):  
Mouse Embryo ◽  
Morphological Characteristics ◽  
Giant Cells ◽  
Mouse Embryos ◽  
Common Origin ◽  
Trophoblast Giant Cells ◽  
Embryonic Ectoderm ◽  
Ectoplacental Cone

Extra-embryonic ectoderm isolated from the mouse embryo as late as 8½ days post coitum can form cells with the morphological characteristics of trophoblast giant cells both in ectopic sites and in vitro. This similarity to the properties of ectoplacental cone tissue provides further support for the postulated common origin of both tissues from the trophectoderm of the blastocyst.

scholarly journals Plac1 Expression Pattern at the Mouse Fetomaternal Interface and Involvement in Trophoblast Differentiation

2017 ◽  
Vol 43 (5) ◽  
pp. 2001-2009 ◽  
Author(s):  
Yanli Gu ◽  
Junhui Wan ◽  
Lv Yao ◽  
Nan-Ni Peng ◽  
Wen-Lin Chang
Keyword(s):  
Expression Pattern ◽  
Giant Cells ◽  
Specific Gene ◽  
Trophoblast Differentiation ◽  
Spatiotemporal Expression ◽  
Trophoblast Stem Cell ◽  
Trophoblast Giant Cells ◽  
Ectoplacental Cone

Background/Aims: It is well known that Plac1 is a placenta-specific gene; however, its spatiotemporal expression pattern and exact role at t h e mouse fetomaternal interface r e m a i n s unclear. Methods: In situ hybridization (ISH) was used to localize the Plac1 mRNA at the mouse fetomaternal interface. A trophoblast stem cell (TS) differentiation model with Plac1 shRNA-overexpressing lentivirus was employed to investigate the possible role of Plac1 in placentation. Real-time RT-PCR was used to detect changes in gene expression. Results: Plac1 was exclusively expressed in the ectoplacental cone (EPC) as well as in 8.5 and 9.5 days post-coitum (dpc) embryos. Subsequently, Plac1 expression was abundant in the spongiotrophoblast layer and moderately in the labyrinth layer until 13.5 dpc, and declined thereafter. Interestingly, Plac1 was also expressed by secondary trophoblast giant cells and glycogen trophoblast cells, but not in primary trophoblast giant cells. Plac1 transcription was increased during the TS differentiation (P < 0.01), and knockdown of Plac1 significantly impaired TS differentiation. Conclusion: Plac1 is abundantly expressed at the fetomaternal interface and in all trophoblast subtypes except in primary trophoblast giant cells. Plac1 knockdown retarded the progress of TS differentiation, indicating that Plac1 is necessary for normal trophoblast differentiation into various trophoblast subpopulations.

scholarly journals Ontogeny of the expression of leptin and its receptor in themurine fetus and placenta

2000 ◽  
Vol 83 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Nigel Hoggard ◽  
Leif Hunter ◽  
Richard G. Lea ◽  
Paul Trayhurn ◽  
Julian G. Mercer
Keyword(s):  
Fetal Development ◽  
Splice Variant ◽  
Leptin Receptor ◽  
Critical Role ◽  
Giant Cells ◽  
Hair Follicles ◽  
Junctional Zone ◽  
Physiological Importance ◽  
Acid Protein ◽  
Trophoblast Giant Cells

Leptin is a 167-amino acid protein that is secreted from adipose cells and expressed in placental tissues. It is important nutritionally in the regulation of energy balance, but also has other functions such as a role in reproduction. To investigate the function of the leptin system in fetal development we examined, primarily by in-situ hybridization and immunohistochemistry, the expression (both mRNA and protein) of leptin and its receptor (including the signalling splice variant) in tissues from 11·5, 13·5, 16·5 and 18·5 d postcoitus murine fetuses and associated placentas. We detected leptin mRNA (at low levels) and protein predominantly in the cytotrophoblasts of the labyrinth part of the placenta, an area of nutrient exchange between the developing fetus and the placenta, and in the trophoblast giant cells situated in the junctional zone at the maternal interface. In addition, leptin was strongly expressed in the fetal cartilage–bone and at a lower level in the hair follicles, heart, and liver of the murine fetus at differing stages of development. The leptin receptor, including the signalling splice variant, was also identified in specific fetal tissues. The physiological importance of expression of both leptin and the leptin receptor (OB-R and OB-Rb) in the placenta remains to be determined. In addition, the high levels of expression of leptin and its receptor in discrete areas of the murine fetus suggest that leptin has a critical role in fetal development.

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