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

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.

Zygote ◽  
2019 ◽  
Vol 27 (1) ◽  
pp. 49-53
Author(s):  
Yuki Maruyama ◽  
Atsushi P. Kimura

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.


2020 ◽  
Vol 11 ◽  
Author(s):  
Qianxia Yu ◽  
Xueyi Tian ◽  
Canjia Lin ◽  
Chelsea D. Specht ◽  
Jingping Liao

The asymmetric flower, lacking any plane of symmetry, is rare among angiosperms. Canna indica L. has conspicuously asymmetric flowers resulting from the presence of a half-fertile stamen, while the other androecial members develop as petaloid staminodes or abort early during development. The molecular basis of the asymmetric distribution of fertility and petaloidy in the androecial whorls remains unknown. Ontogenetic studies have shown that Canna flowers are borne on monochasial (cincinnus) partial florescences within a racemose inflorescence, with floral asymmetry likely corresponding to the inflorescence architecture. Given the hypothesized role of CYC/TB1 genes in establishing floral symmetry in response to the influence of the underlying inflorescence architecture, the spatiotemporal expression patterns of three Canna CYC/TB1 homologs (CiTBL1a, CiTBL1b-1, and CiTBL1b-2) were analyzed during inflorescence and floral development using RNA in situ hybridization and qRT-PCR. In the young inflorescence, both CiTBL1a and CiTBL1b-1 were found to be expressed in the bracts and at the base of the lateral florescence branches, whereas transcripts of CiTBL1b-2 were mainly detected in flower primordia and inflorescence primordia. During early flower development, expression of CiTBL1a and CiTBL1b-1 were both restricted to the developing sepals and petals. In later flower development, expression of CiTBL1a was reduced to a very low level while CiTBL1b-1 was detected with extremely high expression levels in the petaloid androecial structures including the petaloid staminodes, the labellum, and the petaloid appendage of the fertile stamen. In contrast, expression of CiTBL1b-2 was strongest in the fertile stamen throughout flower development, from early initiation of the stamen primordium to maturity of the ½ anther. Heterologous overexpression of CiTBL genes in Arabidopsis led to dwarf plants with smaller petals and fewer stamens, and altered the symmetry of mature flowers. These data provide evidence for the involvement of CYC/TB1 homologs in the development of the asymmetric Cannaceae flower.


2013 ◽  
Vol 41 (3) ◽  
pp. 701-709 ◽  
Author(s):  
Rosalind M. John

A defining feature of mammals is the development in utero of the fetus supported by the constant flow of nutrients from the mother obtained via a specialized organ: the placenta. The placenta is also a major endocrine organ that synthesizes vast quantities of hormones and cytokines to instruct both maternal and fetal physiology. Nearly 20 years ago, David Haig and colleagues proposed that placental hormones were likely targets of the epigenetic process of genomic imprinting in response to the genetic conflicts imposed by in utero development [Haig (1993) Q. Rev. Biol. 68, 495–532]. There are two simple mechanisms through which genomic imprinting could regulate placental hormones. First, imprints could directly switch on or off alleles of specific genes. Secondly, imprinted genes could alter the expression of placental hormones by regulating the development of placental endocrine lineages. In mice, the placental hormones are synthesized in the trophoblast giant cells and spongiotrophoblast cells of the mature placenta. In the present article, I review the functional role of imprinted genes in regulating these endocrine lineages, which lends support to Haig's original hypothesis. I also discuss how imprinting defects in the placenta may adversely affect the health of the fetus and its mother during pregnancy and beyond.


2000 ◽  
Vol 24 (1) ◽  
pp. 95-108 ◽  
Author(s):  
N Sahgal ◽  
GT Knipp ◽  
B Liu ◽  
BM Chapman ◽  
G Dai ◽  
...  

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.


Development ◽  
1981 ◽  
Vol 66 (1) ◽  
pp. 43-55
Author(s):  
J. Rossant ◽  
K. M. Vijh

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.


1991 ◽  
Vol 260 (5) ◽  
pp. F704-F709 ◽  
Author(s):  
A. Vignery ◽  
F. Wang ◽  
H. Y. Qian ◽  
E. J. Benz ◽  
M. Gilmore-Hebert

We previously reported that multinucleated macrophages express a high concentration of Na(+)-K(+)-ATPases that are concentrated on the nonadherent domain of their plasma membrane (A. Vignery, T. Niven-Fairchild, D. H. Ingbar, and M. Caplan. J. Histochem. Cytochem. 37: 1265-1271, 1989). We also showed that an increase in newly synthesized alpha-subunit occurred during cell culture and multinucleation. We now present evidence that macrophage multinucleation in vitro is accompanied by an increased accumulation of Na(+)-K(+)-ATPase alpha-subunit mRNA. Most interesting is the detection of significant amount of both alpha 1- and alpha 3-isoform mRNA and peptide in these cells by in situ hybridization, Northern and Western blot analyses. These qualitative and quantitative variations in Na(+)-K(+)-ATPase expression suggest that macrophage multinucleation is accompanied by a coordinated regulation of gene expression and that multinucleation confers a specific function to macrophages. Multinucleated macrophages offer a novel model system to investigate not only the specific function(s) of the alpha 3-isoform but also the role of the Na(+)-K(+)-ATPase in giant cells and osteoclasts.


2004 ◽  
Vol 16 (3) ◽  
pp. 301 ◽  
Author(s):  
Karl Klisch ◽  
Preben D. Thomsen ◽  
Vibeke Dantzer ◽  
Rudolf Leiser

The frequency of polyploidisation in bovine binucleate trophoblast giant cells (TGC) from placentomes (PL) and the interplacentomal allantochorion (AL) of six male fetuses with a crown–rump length between 3.5 and 103 cm was determined by in situ hybridisation with a chromosome-7-specific probe, using a probe specific for the Y chromosome to distinguish between maternal and fetal nuclei. The results showed that polyploid nuclei were essentially always of fetal origin. The frequency of tetraploid nuclei varied between 3% and 15% in both the placentomal and interplacentomal samples, with mean frequencies of 8.8% and 10.0% respectively. Octoploid nuclei were observed with a mean frequency of 1.1% in the interplacentomal samples, but were absent in samples from placentomes. Subsequent determination of nuclear DNA content by cytophotometric measurement of Feulgen-stained nuclei revealed that the frequency of nuclei with an 8C DNA content was several fold higher (AL 5.4%; PL 7.8%) than the frequency of octoploidy, suggesting that tetraploid TGC cells are arrested in the G2 phase of the cell cycle.


PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254674
Author(s):  
Hiromu Morimoto ◽  
Misuzu Ueno ◽  
Hideyuki Tanabe ◽  
Tomohiro Kono ◽  
Hidehiko Ogawa

Trophoblast giant cells (TGCs), a mouse trophoblast subtype, have large amounts of cytoplasm and high ploidy levels via endocycles. The diverse functions and gene expression profiles of TGCs have been studied well, but their nuclear structures remain unknown. In this study, we focus on Lamin B1, a nuclear lamina, and clarify its expression dynamics, regulation and roles in TGC functions. TGCs that differentiated from trophoblast stem cells were used. From days 0 to 9 after differentiation, the number of TGCs gradually increased, but the amount of LMNB1 peaked at day 3 and then slightly decreased. An immunostaining experiment showed that LMNB1-depleted TGCs increased after day 6 of differentiation. These LMNB1-depleted TGCs diffused peripheral localization of the heterochromatin marker H3K9me2 in the nuclei. However, LMINB1-knock down was not affected TGCs specific gene expression. We found that the death of TGCs also increased after day 6 of differentiation. Moreover, Lamin B1 loss and the cell death in TGCs were protected by 10−6 M progesterone. Our results conclude that progesterone protects against Lamin B1 loss and prolongs the life and function of TGCs.


2004 ◽  
Vol 16 (9) ◽  
pp. 271
Author(s):  
P. Murthi ◽  
M. D. Bates ◽  
G. Sankaran ◽  
S. P. Brennecke ◽  
B. Kalionis

In a screen for homeobox genes in the human placenta, we cloned and characterised HLX1 (also known as HB24) (1). Furthermore, we provided evidence that HLX1 may be a regulator of human placental develolpment (2). We have since shown that the mouse homologue of HLX1, called Hlx, is expressed in the murine placenta. In situ mRNA hybridisation studies and antibody localisation of Hlx revealed expression in the labyrinth layer (LL), secondary giant cells (GC) and in the spongiotrophoblast layer (STL) (3). The STL is required for structural support of the placenta. Targeted gene mutation of Hlx resulted in embryonic defects in the developing gut and the liver (4) but the effects on placental development were not investigated. Histological preparations of placental tissues collected from Days 10.5, 13.5 and 19.5 from Hlx mutant mice were investigated for morphological changes. Our preliminary observations reveal that by haematoxylin and eosin staining the STL of the mutant murine placenta is severely disrupted but the overlying GC layer appears to be unaffected. Endogenous alkaline phosphatase staining of the LL further confirmed that the highly vascularised LL where fetal- maternal exchange occurs, is disorganised and expands into the region normally occupied by the STL. These observations indicate that Hlx is essential for normal placental development. (1) Quinn LM, Kalionis B. (1997) Gene 187, 55–61. (2) Quinn LM, Kalionis B. (1997) Repro. Dev. 9, 617–623. (3) Johnson B (1999) PhD Thesis, University of Adelaide. (4) Hentsch B, Harvey RP (1996) Gene Dev. 10, 70–79.


Development ◽  
1997 ◽  
Vol 124 (4) ◽  
pp. 907-914 ◽  
Author(s):  
G.T. Ma ◽  
M.E. Roth ◽  
J.C. Groskopf ◽  
F.Y. Tsai ◽  
S.H. Orkin ◽  
...  

We previously demonstrated that the zinc finger transcription factors GATA-2 and GATA-3 are expressed in trophoblast giant cells and that they regulate transcription from the mouse placental lactogen I gene promoter in a transfected trophoblast cell line. We present evidence here that both of these factors regulate transcription of the placental lactogen I gene, as well as the related proliferin gene, in trophoblast giant cells in vivo. Placentas lacking GATA-3 accumulate placental lactogen I and proliferin mRNAs to a level 50% below that reached in the wild-type placenta. Mutation of the GATA-2 gene had a similar effect on placental lactogen I expression, but led to a markedly greater reduction (5- to 6-fold) in proliferin gene expression. Placentas lacking GATA-2 secrete significantly less angiogenic activity than wild-type placentas as measured in an endothelial cell migration assay, consistent with a reduction in expression of the angiogenic hormone proliferin. Furthermore, within the same uterus the decidual tissue adjacent to mutant placentas displays markedly reduced neovascularization compared to the decidual tissue next to wild-type placentas. These results indicate that GATA-2 and GATA-3 are important in vivo regulators of trophoblast-specific gene expression and placental function, and reveal a difference in the effect of these two factors in regulating the synthesis of related placental hormones.


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