scholarly journals O-GlcNAc modification mediates aquaporin 3 to coordinate endometrial cell glycolysis and affects embryo implantation

2021 ◽  
Author(s):  
Hongshuo Zhang ◽  
Jia Qi ◽  
Jingyuan Pei ◽  
Man Zhang ◽  
Yuhong Shang ◽  
...  
Keyword(s):  
Embryo Implantation ◽  
Endometrial Cell ◽  
Aquaporin 3

scholarly journals Endometrial cell-derived small extracellular vesicle miR-100-5p promotes functions of trophoblast during embryo implantation

2021 ◽  
Vol 23 ◽  
pp. 217-231
Author(s):  
Qiang Tan ◽  
Shuang Shi ◽  
Jingjie Liang ◽  
Dingren Cao ◽  
Shaoyu Wang ◽  
...  
Keyword(s):  
Embryo Implantation ◽  
Extracellular Vesicle ◽  
Endometrial Cell

scholarly journals Fatty Acid-Binding Protein 4 in Endometrial Epithelium Is Involved in Embryonic Implantation

2017 ◽  
Vol 41 (2) ◽  
pp. 501-509 ◽  
Author(s):  
Peng Wang ◽  
Qiuyuan Zhu ◽  
Huilian Peng ◽  
Mengkai Du ◽  
Minyue Dong ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Epithelial Cell ◽  
Pregnancy Loss ◽  
Fatty Acid Binding Protein ◽  
Embryo Implantation ◽  
Endometrial Cell ◽  
Fatty Acid Binding ◽  
Endometrial Epithelial Cell ◽  
Acid Binding Protein ◽  
Icr Mice

Aims: To clarify the role of fatty acid-binding protein 4 (FABP4) of endometrial epithelial cell in the establishment and maintenance of pregnancy and the involvement in the pathogenesis of pregnancy loss. Methods: The expression of FABP4 and uterine receptive factor (LIF, Integrin-β3 and Claudin 4) was determined by Western blotting or quantitative PCR. FABP4 siRNA was used to silence FABP4 while FABP4 inhibitor was used to inhibit the function of FABP4 in endometrial epithelial cell. ICR mice were raised to evaluate the effect of FABP4 silence or inhibition on embryo implantation in vivo after FABP4 siRNA mixture or inhibitor was injected into uterus, and an embryonic adhesion system using trophoblast spheroids mimicking embryos was set up to assess the effect of FABP4 silence or inhibition on embryonic adhesion onto endometrial cell in vitro. Results: The expression of FABP4 mRNA was significantly decreased in the deciduas of women with pregnancy loss compared with that of women with normal pregnancy. FABP4 siRNA significantly reduced the number of embryos implanted and FABP4 expression in ICR mice. FABP4 inhibition also significantly decreased the number of embryos implanted. Either silence or inhibition of FABP4 in endometrial epithelial cell abolished the expression of uterine receptive factors induced by the combination of estrogen and progesterone-induced, and reduced the number of trophoblast spheroids adhered onto endometrial cell. Conclusions: FABP4 regulates embryo implantation via altering uterine receptivity and decreased expression of FABP4 in endometrium may be linked with pregnancy loss, indicating FABP4 has biological role in the establishment and maintenance of pregnancy and subsequently is involved in pathogenesis of pregnancy loss.

Inhibition of TMEM16A impedes embryo implantation and decidualization in mice

Reproduction ◽  
2018 ◽  
Author(s):  
Qianrong Qi ◽  
Yifan Yang ◽  
Kailin Wu ◽  
Qingzhen Xie
Keyword(s):  
Progesterone Receptor ◽  
Stromal Cells ◽  
Embryo Implantation ◽  
Mouse Uterus ◽  
Endometrial Stromal Cells ◽  
Uterine Endometrium ◽  
Molecule Inhibitor ◽  
Pathway Inhibition ◽  
And Function ◽  
Reproductive Processes

Recent studies revealed that TMEM16A is involved in several reproductive processes, including ovarian estrogen secretion and ovulation, sperm motility and acrosome reaction, fertilization, and myometrium contraction. However, little is known about the expression and function of TMEM16A in embryo implantation and decidualization. In this study, we focused on the expression and regulation of TMEM16A in mouse uterus during early pregnancy. We found that TMEM16A is up-regulated in uterine endometrium in response to embryo implantation and decidualization. Progesterone treatment could induce TMEM16A expression in endometrial stromal cells through progesterone receptor/c-Myc pathway, which is blocked by progesterone receptor antagonist or the inhibitor of c-Myc signaling pathway. Inhibition of TMEM16A by small molecule inhibitor (T16Ainh-A01) resulted in impaired embryo implantation and decidualization in mice. Treatment with either specific siRNA of Tmem16a or T16Ainh-A01 inhibited the decidualization and proliferation of mouse endometrial stromal cells. In conclusion, our results revealed that TMEM16A is involved in embryo implantation and decidualization in mice, compromised function of TMEM16A may lead to impaired embryo implantation and decidualization.

Non-coding RNAs and embryo implantation

10.2741/e313 ◽  
2011 ◽  
Vol E3 (3) ◽  
pp. 1092-1099
Author(s):  
Zeng-Ming Yang
Keyword(s):  
Embryo Implantation ◽  
Non Coding Rnas
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