scholarly journals Evidence of embryonic regulation of maternally derived yolk corticosterone

2018 ◽  
Vol 221 (22) ◽  
pp. jeb182600 ◽  
Author(s):  
Amanda W. Carter ◽  
Rachel M. Bowden ◽  
Ryan T. Paitz
Keyword(s):  
1998 ◽  
Vol 5 (1) ◽  
pp. 117A-117A ◽  
Author(s):  
P CABALLEROCAMPO ◽  
A BERNAL ◽  
A MERCADER ◽  
E OCONNOR ◽  
J COLOMA ◽  
...  

1999 ◽  
Vol 14 (Suppl_3) ◽  
pp. 69-70
Author(s):  
P. Caballero-Campo ◽  
M. Meseguer ◽  
J.C. Martín ◽  
J. Coloma ◽  
J.E. O'Connor ◽  
...  

2011 ◽  
Vol 11 ◽  
pp. 1770-1780 ◽  
Author(s):  
Daisuke Sugiyama ◽  
Tomoko Inoue-Yokoo ◽  
Stuart T. Fraser ◽  
Kasem Kulkeaw ◽  
Chiyo Mizuochi ◽  
...  

Hematopoietic stem cells (HSCs) can differentiate into several types of hematopoietic cells (HCs) (such as erythrocytes, megakaryocytes, lymphocytes, neutrophils, or macrophages) and also undergo self-renewal to sustain hematopoiesis throughout an organism's lifetime. HSCs are currently used clinically as transplantation therapy in regenerative medicine and are typically obtained from healthy donors or cord blood. However, problems remain in HSC transplantation, such as shortage of cells, donor risks, rejection, and graft-versus-host disease (GVHD). Thus, increased understanding of HSC regulation should enable us to improve HSC therapy and develop novel regenerative medicine techniques. HSC regulation is governed by two types of activity: intrinsic regulation, programmed primarily by cell autonomous gene expression, and extrinsic factors, which originate from so-called “niche cells” surrounding HSCs. Here, we focus on the latter and discuss HSC regulation with special emphasis on the role played by niche cells.


1999 ◽  
Vol 17 (03) ◽  
pp. 267-274 ◽  
Author(s):  
Carlos Simón ◽  
Julio Martín ◽  
Arancha Galan ◽  
Diana Valbuena ◽  
Antonio Pellicer
Keyword(s):  

1997 ◽  
Vol 82 (8) ◽  
pp. 2607-2616 ◽  
Author(s):  
Carlos Simón ◽  
MarÍa José Gimeno ◽  
Amparo Mercader ◽  
José Enrique O’Connor ◽  
José RemohÍ ◽  
...  

In the present study, we examined the embryonic regulation ofβ 3 integrin in human endometrial epithelial cells (EEC) at the protein level and analyzed putative embryonic factors responsible for this regulation. The model employed is based on a clinical in vitro fertilization program in which single human embryos were cocultured with EEC until blastocyst stage and then transferred back to the uterus. After embryo transfer, EEC wells were divided according to the embryonic status reached: EEC with embryos that achieved the blastocyst stage, EEC with arrested embryos, and EEC without embryos. Immunostaining for β3 was positive in plasma membrane of EEC. Flow cytometry showed a mean percentage ofβ 3-stained cells of 24.1 ± 5.7 in EEC cocultured with embryos that achieved the blastocyst stage (n = 13) vs. 9.5 ± 1.6 (P < 0.05) in those EEC cultured with arrested embryos (n = 12). Immunostaining for α1 and α4 integrins was negative in EEC monolayers studied, regardless of the presence or absence of embryos, and these findings were confirmed by flow cytometry. The possibility that the embryonic IL-1 system and leukemia inhibitory factor were involved in the endometrial β3 up-regulation was investigated by neutralizing experiments demonstrating a significant inhibition of β3-stained cells when EEC monolayers were cultured in the presence of EEC/blastocyst-conditioned media with (n = 4) vs. without (n = 8) antihuman interleukin (IL)-1α + IL-1β (1.65% vs. 14.6%; P < 0.05). Dose-response experiments further demonstrated an up-regulation of β3 positive cells when IL-1α + IL-1β were added to the medium at a concentration of 10 pg/mL compared with control medium without added cytokines (40% vs. 20%, n = 4). The functional relevance of the EEC β3 up-regulation was tested using a mouse blastocyst adhesion assay. More mouse blastocysts attached to EEC previously in contact with human blastocyst (72.7%) compared with those EEC previously in contact with arrested embryos (40%). Our results demonstrate the selective effect of a developing human embryo on EEC expression of β3, which is maximal when a human blastocyst instead of an arrested embryo is considered. Furthermore, the embryonic IL-1 system seems to be involved in the EECβ 3 up-regulation, reinforcing the concept of precise paracrine cross-talk between blastocyst and endometrial epithelium during embryonic implantation.


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