Lipoxin A4 interferes with embryo implantation via suppression of epithelial‐mesenchymal transition

2019 ◽  
Vol 81 (5) ◽  
pp. e13107 ◽  
Author(s):  
Zhangye Xu ◽  
Shenzhi Zhao ◽  
Tong Zhou ◽  
Tingting Liao ◽  
Xianping Huang ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Embryo Implantation ◽  
Lipoxin A4 ◽  
Mesenchymal Transition

Adenomyosis – its possible effect on endometrial function and receptivity

2021 ◽  
Vol 86 (3) ◽  
pp. 205-209
Author(s):  
Karel Crha ◽  
◽  
Michal Ješeta ◽  
Radovan Pilka ◽  
Pavel Ventruba ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Current Knowledge ◽  
Histopathological Examination ◽  
Transvaginal Ultrasound ◽  
Embryo Implantation ◽  
Diagnostic Methods ◽  
Mesenchymal Transition ◽  
New Information

Summary Objective: There have been many studies on adenomyosis, which can impair the quality of life of a woman. There are various kinds of opinions on the pathogenesis, diagnostics and treatment of adenomyosis. The goal of this article is to present the current knowledge of adenomyosis and its impact on the endometrial function and receptivity. Methods: PubMed/Medline, Web of Sciences and Scopus were searched for the articles in English indexed until February 2021 with terms of: adenomyosis, endometrial receptivity, and infertility. Results: Recent studies on angiogenesis and epithelial-mesenchymal transition in the endometrium bring new information on the ethiology and pathogenesis of adenomyosis. In clinical practice, the main diagnostic methods of adenomyosis include transvaginal ultrasound, magnetic resonance imaging or hysteroscopy, although the definitive confirmation is set by histopathological examination. The rules of #Enzian classification of endometriosis should be applied for the classification of adenomyosis. The treatment of adenomyosis should consider individual clinical presentation and reproductive plans of a patient and should be performed in centers for the treatment of endometriosis. Conclusion: Adenomyosis affects endometrial vascularisation and epithelial-mesenchymal transition/mesenchymal-epithelial transition; thus, it can be the cause of irregular uterine bleeding or embryo implantation failure. The research and analysis of endometrial proteome could lead to the new ways of adenomyosis treatment.

Epithelial-mesenchymal transition process during embryo implantation

2022 ◽  
Author(s):  
Farnaz Oghbaei ◽  
Reza Zarezadeh ◽  
Davoud Jafari-Gharabaghlou ◽  
Minoo Ranjbar ◽  
Mohammad Nouri ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Embryo Implantation ◽  
Transition Process ◽  
Mesenchymal Transition

Lipoxin A4 Suppresses Estrogen-Induced Epithelial–Mesenchymal Transition via ALXR-Dependent Manner in Endometriosis

2017 ◽  
Vol 25 (4) ◽  
pp. 566-578 ◽  
Author(s):  
Rong-Feng Wu ◽  
Zhi-Xiong Huang ◽  
Jing Ran ◽  
Song-Juan Dai ◽  
Dian-Chao Lin ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Dependent Manner ◽  
Lipoxin A4 ◽  
Mesenchymal Transition

Role of epithelial–mesenchymal transition regulated by twist basic helix-loop-helix transcription factor 2 (Twist2) in embryo implantation in mice

2019 ◽  
Vol 31 (5) ◽  
pp. 932
Author(s):  
Jinhai Gou ◽  
Tingwenyi Hu ◽  
Lin Li ◽  
Luqi Xue ◽  
Xia Zhao ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Western Blot ◽  
Epithelial Mesenchymal Transition ◽  
Embryo Implantation ◽  
Mesenchymal Transition ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix ◽  
Implantation Sites ◽  
E Cadherin

In a previous study we found the expression of epithelial–mesenchymal transition (EMT) biomarkers, including E-cadherin and N-cadherin, was significantly altered in uterine endometrium during embryo implantation via regulation by microRNA (miRNA)-429 and protocadherin-8 (Pcdh8). As a natural continuation of the previous study, the aim of the present study was to explore the role of EMT during embryo implantation and the potential activity of twist basic helix-loop-helix transcription factor 2 (Twist2) in regulating embryo implantation. A pregnancy model was established by naturally mating adult female ICR mice with fertile males. A pseudopregnancy model was established by mating fertile female ICR mice with vasectomised males. An invitro model of embryo implantation was established by the coculture of Ishikawa and JAR spheroids. Endometrial tissue during the peri-implantation period was collected, as were Ishikawa cells, JAR cells and cocultured cells. The expression of EMT markers (E-cadherin, N-cadherin, vimentin and cytokeratin) and Twist2 was detected invivo and invitro using the western blot analysis during embryo implantation. The expression of N-cadherin and vimentin (mesenchymal markers) was upregulated in the invitro implantation model, with downregulation of E-cadherin and cytokeratin (epithelial markers) expression. The expression of N-cadherin, vimentin and Twist2 increased significantly at the implantation sites at the time of implantation (Day 5), whereas the expression of E-cadherin and cytokeratin decreased. Location of Twist2 during embryo implantation was detected by immunohistochemistry (IHC), which revealed that it was extensively expressed in endometrial glandular epithelium and luminal epithelium at implantation sites on Day 5. The effect of the expression of Twist2 on embryo implantation was evaluated by suppressing Twist2 using Twist2-short interference (si) RNA in invivo and invitro models. The numbers of implanted embryos and the implantation rate were compared invivo and invitro. Western blot analysis showed that suppression of Twist2 led to upregulation of E-cadherin and cytokeratin, accompanied by downregulation of N-cadherin and vimentin (P<0.05). The number of implanted embryos after Twist2-siRNA interference was lower than in normal pregnancy (mean (±s.d.) 2.4±0.5 vs 6.8±1.3 respectively; P<0.05). These findings suggest the involvement of EMT in embryo implantation. The suppression of Twist2 could suppress embryo implantation by regulating EMT.

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