Homeobox gene HB24, a regulator of haematopoiesis, is a candidate for regulating differentiation of the extra-embryonic trophoblast cell lineage

1997 ◽  
Vol 9 (6) ◽  
pp. 617 ◽  
Author(s):  
L. M. Quinn ◽  
S. E. Latham ◽  
B. Kalionis

Expression of the human homeobox gene HB24 in the cytotrophoblast stem cell population in rst-trimester human placenta was investigated. HB24expression was downregulated after cytotrophoblast had differentiated into syncytiotrophoblast. Expression of HB24 was also detected in rst-trimester invasive extravillous cytotrophoblast cells. In term placenta, HB24 expression was detected in residual cytotrophoblast cells and in syncytiotrophoblast. Northern analysis revealed two HB24 transcripts in rst-trimester placenta of approximately 2·5 kb and 5·3 kb. Ribonuclease protection assays were used to conrm expression of HB24 in rst-trimester and term placenta and also to provide evidence that HB24 is downregulated in choriocarcinoma cell lines. In addition to being required for differentiation of the haematopoietic cell lineage, HB24 may be required for differentiation of the extra-embryonic trophoblast cell lineage.


Author(s):  
A. C. Enders

The alteration in membrane relationships seen at implantation include 1) interaction between cytotrophoblast cells to form syncytial trophoblast and addition to the syncytium by subsequent fusion of cytotrophoblast cells, 2) formation of a wide variety of functional complex relationships by trophoblast with uterine epithelial cells in the process of invasion of the endometrium, and 3) in the case of the rabbit, fusion of some uterine epithelial cells with the trophoblast.Formation of syncytium is apparently a membrane fusion phenomenon in which rapid confluence of cytoplasm often results in isolation of residual membrane within masses of syncytial trophoblast. Often the last areas of membrane to disappear are those including a desmosome where the cell membranes are apparently held apart from fusion.



Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e16-e17
Author(s):  
Kaela M. Varberg ◽  
Boryana Koseva ◽  
Khursheed Iqbal ◽  
Jinchu Vijay ◽  
Rebecca Biswell ◽  
...  


Placenta ◽  
2019 ◽  
Vol 83 ◽  
pp. e118
Author(s):  
Milena Mirandola ◽  
Jady Rabelo ◽  
Carla Bandeira ◽  
Marco Amadeu ◽  
Estela Bevilacqua


2019 ◽  
Vol 25 (9) ◽  
pp. 572-585 ◽  
Author(s):  
Lynda K Harris ◽  
Priyadarshini Pantham ◽  
Hannah E J Yong ◽  
Anita Pratt ◽  
Anthony J Borg ◽  
...  

Abstract Fetal growth restriction (FGR) is caused by poor placental development and function early in gestation. It is well known that placentas from women with FGR exhibit reduced cell growth, elevated levels of apoptosis and perturbed expression of the growth factors, cytokines and the homeobox gene family of transcription factors. Previous studies have reported that insulin-like growth factor-2 (IGF2) interacts with its receptor-2 (IGF2R) to regulate villous trophoblast survival and apoptosis. In this study, we hypothesized that human placental IGF2R-mediated homeobox gene expression is altered in FGR and contributes to abnormal trophoblast function. This study was designed to determine the association between IGF2R, homeobox gene expression and cell survival in pregnancies affected by FGR. Third trimester placentas were collected from FGR-affected pregnancies (n = 29) and gestation matched with control pregnancies (n = 30). Functional analyses were then performed in vitro using term placental explants (n = 4) and BeWo trophoblast cells. mRNA expression was determined by real-time PCR, while protein expression was examined by immunoblotting and immunohistochemistry. siRNA transfection was used to silence IGF2R expression in placental explants and the BeWo cell-line. cDNA arrays were used to screen for downstream targets of IGF2R, specifically homeobox gene transcription factors and apoptosis-related genes. Functional effects of silencing IGF2R were then verified by β-hCG ELISA, caspase activity assays and a real-time electrical cell-impedance assay for differentiation, apoptosis and cell growth potential, respectively. IGF2R expression was significantly decreased in placentas from pregnancies complicated by idiopathic FGR (P < 0.05 versus control). siRNA-mediated IGF2R knockdown in term placental explants and the trophoblast cell line BeWo resulted in altered expression of homeobox gene transcription factors, including increased expression of distal-less homeobox gene 5 (DLX5), and decreased expression of H2.0-Like Homeobox 1 (HLX) (P < 0.05 versus control). Knockdown of IGF2R transcription increased the expression and activity of caspase-6 and caspase-8 in placental explants, decreased BeWo proliferation and increased BeWo differentiation (all P < 0.05 compared to respective controls). This is the first study linking IGF2R placental expression with changes in the expression of homeobox genes that control cellular signalling pathways responsible for increased trophoblast cell apoptosis, which is a characteristic feature of FGR.



1996 ◽  
Vol 16 (2) ◽  
pp. 205-210 ◽  
Author(s):  
G Quinn ◽  
D S W Boam ◽  
J R E Davis ◽  
J D Glazier ◽  
P Mylona ◽  
...  

ABSTRACT A transcriptional enhancer which has a consensus binding sequence for transcription enhancer factor-1 (TEF-1) has been found 3′ of the hPL3 gene. We examined whether TEF-1 is expressed by the human placenta and whether such expression is co-ordinated with that of human placental lactogen (hPL). Probing Northern blots of total RNA from first trimester and term placenta, the choriocarcinoma-derived cell line JAr and primary cultured cytotrophoblast cells with a cDNA for TEF-1 revealed transcripts of 12–13 kb and 3–4 kb. The level of TEF-1 expression was the same in first trimester as compared with term placenta and in undifferentiated JAr as compared with differentiated cytotrophoblast cells. hPL expression was tenfold higher in term compared with first trimester placenta and, whilst detectable in cytotrophoblast cells, was undetectable in JAr cells. These data show that TEF-1 is expressed by the placenta but is not co-ordinated with hPL expression.





Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e53-e54
Author(s):  
Keisuke Kozai ◽  
Vinay Shukla ◽  
Michael J. Soares


2014 ◽  
Vol 58 (2-3-4) ◽  
pp. 231-238 ◽  
Author(s):  
Satoshi Tanaka ◽  
Momo O. Nakanishi ◽  
Kunio Shiota


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