Genome Multiplication in Trophoblast Giant Cells of Sheep, Goat, Water Buffalo and Deer: an Image Cytophotometric Study

2000 ◽  
Vol 35 (3-4) ◽  
pp. 145-148 ◽  
Author(s):  
K Klisch ◽  
G Schuler ◽  
MA Miglino ◽  
R Leiser
Keyword(s):  
Water Buffalo ◽  
Giant Cells ◽  
Cytophotometric Study ◽  
Trophoblast Giant Cells

Binucleate trophoblast giant cells in the water buffalo (Bubalus bubalis) placenta

2005 ◽  
Vol 267 (1) ◽  
pp. 50-56 ◽  
Author(s):  
A.F. Carvalho ◽  
K. Klisch ◽  
M.A. Miglino ◽  
F.T.V. Pereira ◽  
E. Bevilacqua
Keyword(s):  
Water Buffalo ◽  
Giant Cells ◽  
Bubalus Bubalis ◽  
Trophoblast Giant Cells

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.

Replication Timing Predicts Underreplicated Domains in Polyploid Trophoblast Giant Cells

Placenta ◽  
2013 ◽  
Vol 34 (9) ◽  
pp. A8
Author(s):  
Roberta Hannibal ◽  
Edward Chuong ◽  
Juan Carlos Rivera Mulia ◽  
David Gilbert ◽  
Anton Valouev ◽  
...  
Keyword(s):  
Replication Timing ◽  
Giant Cells ◽  
Trophoblast Giant Cells

Parp-1deficiency in ES cells promotes invasive and metastatic lesions accompanying induction of trophoblast giant cells during tumorigenesis in uterine environment

2013 ◽  
Vol 63 (8) ◽  
pp. 408-414 ◽  
Author(s):  
Tadashige Nozaki ◽  
Hiroaki Fujimori ◽  
Junhui Wang ◽  
Hiroshi Suzuki ◽  
Hiroshi Imai ◽  
...  
Keyword(s):  
Es Cells ◽  
Giant Cells ◽  
Metastatic Lesions ◽  
Uterine Environment ◽  
Trophoblast Giant Cells

scholarly journals A molecular mechanism of mouse placental spongiotrophoblast differentiation regulated by prolyl oligopeptidase

Zygote ◽  
2019 ◽  
Vol 27 (1) ◽  
pp. 49-53
Author(s):  
Yuki Maruyama ◽  
Atsushi P. Kimura
Keyword(s):  
Molecular Mechanism ◽  
Critical Role ◽  
Specific Inhibitor ◽  
Cell Types ◽  
Giant Cells ◽  
Akt Pathway ◽  
Prolyl Oligopeptidase ◽  
Trophoblast Stem ◽  
Trophoblast Stem Cell ◽  
Trophoblast Giant Cells

SummaryIn eutherian mammals, the placenta plays a critical role in embryo development by supplying nutrients and hormones and mediating interaction with the mother. To establish the fine connection between mother and embryo, the placenta needs to be formed normally, but the mechanism of placental differentiation is not fully understood. We previously revealed that mouse prolyl oligopeptidase (POP) plays a role in trophoblast stem cell (TSC) differentiation into two placental cell types, spongiotrophoblasts (SpT) and trophoblast giant cells. Here, we focused on SpT differentiation and attempted to elucidate a molecular mechanism. ForAscl2,Arnt, andEgfrgenes that are indispensable for SpT formation, we found that a POP-specific inhibitor, SUAM-14746, significantly decreasedAscl2expression, which was consistent with a significant decrease in expression ofFlt1, a gene downstream ofAscl2. Although this downregulation was unlikely to be mediated by the PI3K-Akt pathway, our results indicated that POP controls TSC differentiation into SpT by regulating theAscl2gene.

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