Leukemia inhibitory factor enhanced the developmental and implantation compatibility of mouse embryos in co-culture with human endometrial epithelial cells

2021 ◽  
Vol 0 (0) ◽  
pp. 0
Author(s):  
Mehrdad Bakhtiyari ◽  
Ali Hosseini ◽  
Bahar Movaghar ◽  
ShowraAmani Abkenari ◽  
Hassan Nazari
Endocrinology ◽  
2009 ◽  
Vol 150 (6) ◽  
pp. 2915-2923 ◽  
Author(s):  
M. Marwood ◽  
K. Visser ◽  
L. A. Salamonsen ◽  
E. Dimitriadis

Embryo implantation requires the closely harmonized processes of apposition, attachment, and adhesion of the conceptus to the maternal endometrial epithelium. IL-11 and leukemia inhibitory factor (LIF), two IL-6 family cytokines, are produced by the endometrium and are absolutely required for implantation in mice. We examined the effect of IL-11 and LIF on human endometrial epithelial cell adhesion. Both cytokines increased adhesion of primary human endometrial epithelial cells to fibronectin and collagen IV. IL-11 stimulated, whereas LIF had no effect on the adhesion of trophoblast to endometrial epithelial cells. Focused oligogene arrays were used to identify extracellular matrix and adhesion molecules mRNAs regulated by endometrial epithelial cells. We demonstrated by real-time RT-PCR and antibody arrays that both cytokines increased integrin-α2 mRNA and protein by endometrial epithelial cells. Signal transducers and activators of transcription (STAT)-3 inhibition reduced IL-11- and LIF-mediated epithelial cell adhesion to fibronectin, suggesting both cytokines regulated adhesion via phosphorylation of STAT3. Addition of either IL-11 neutralizing antibody and IL-11 or LIF and LIF antagonist to endometrial epithelial cells abolished cytokine induced phosphorylated STAT3. LIF but not IL-11 induced adhesion to collagen IV was reduced by an integrin-α2β1 neutralizing antibody. This study demonstrated that IL-11 and LIF regulated endometrial epithelial cell adhesion, suggesting that targeting IL-11 and LIF may be useful in regulating fertility by either enhancing or blocking implantation.


Neuroreport ◽  
2006 ◽  
Vol 17 (18) ◽  
pp. 1863-1866 ◽  
Author(s):  
Toshihisa Hatta ◽  
Akihiro Matsumoto ◽  
Atsuki Ono ◽  
Jun Udagawa ◽  
Masayuki Nimura ◽  
...  

1992 ◽  
Vol 89 (17) ◽  
pp. 8195-8199 ◽  
Author(s):  
F. Conquet ◽  
N. Peyrieras ◽  
L. Tiret ◽  
P. Brulet

2007 ◽  
Vol 196 (2) ◽  
pp. 425-433 ◽  
Author(s):  
Jin-Wen Xu ◽  
Naomi Yasui ◽  
Katsumi Ikeda ◽  
Wei-Jun Pan ◽  
June Watanabe ◽  
...  

Isoflavones have attracted much attention due to their association with health benefits; however, comprehensive understanding of the beneficial impacts of isoflavones on uterine biology at the molecular level remains unexplored. In the present study, our data showed that isoflavones aglycones AglyMax, genistein, and equol, but not daidzein, within the range of plasma concentration, displayed bioavailability in regulating the secretion of leukemia inhibitory factor (LIF) and transforming growth factor β (TGF-β) in Ishikawa cells, which was blocked by an estrogen receptor antagonist ICI 182 780, mitogen-activated protein kinase kinase (MEK)1/2 inhibitor PD98059, and p38 mitogen-activated protein kinase inhibitor SB203580. We also found that AglyMax and genistein increased in cyclic AMP release and the expression of glycodelin protein in Ishikawa cells assayed using western blot and immunochemical staining. The MEK1/2 inhibitor PD98059 and the protein kinase A inhibitor H89, but not SB203580, attenuated this glycoprotein expression. Moreover, isoflavone aglycones AglyMax stimulated LIF, and TGF-β secretion, and glycodelin expression in separate primary endometrial epithelial cells in the follicular phase or luteal phase from healthy subject donors. Overall, our findings suggest that isoflavones may alter the uterine expression of estrogen-responsive genes.


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