The Mesenchymal—Epithelial Transition During In Vitro Decidualization

Zhang, Xiuhong; Liang, Xuan; Liang, Xiao-Huan; Wang, Tong-Song; Qi, Qian-Rong; Deng, Wenbo; Sha, Aihua; Yang, Zeng‐Ming

doi:10.1177/1933719112472738

Cited by 68 publications

(62 citation statements)

References 27 publications

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“…8). Our results are strongly supported by the recent observation that MET occurs during decidualization when fibroblast-like endometrial stromal cells are converted into polygonal epithelium (Zhang et al, 2013). The colocalization of STAT3 with MCL-1 is clearly evident in stromal cells at the post-implantation stage, which is in line with the onset of decidualization.…”

Section: Discussionsupporting

confidence: 79%

STAT3 and MCL-1 associate to cause a mesenchymal epithelial transition

Renjini

Titus

Narayan

et al. 2014

Journal of Cell Science

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Embryo implantation is effected by a myriad of signaling cascades acting on the embryo-endometrium axis. Here we show, by using MALDI TOF analysis, far-western analysis and colocalization and co-transfection studies, that STAT3 and MCL-1 are interacting partners during embryo implantation. We show in vitro that the interaction between the two endogenous proteins is strongly regulated by estrogen and progesterone. Implantation, pregnancy and embryogenesis are distinct from any other process in the body, with extensive, but controlled, proliferation, cell migration, apoptosis, cell invasion and differentiation. Cellular plasticity is vital during the early stages of development for morphogenesis and organ homeostasis, effecting the epithelial to mesenchymal transition (EMT) and, the reverse process, mesenchymal to epithelial transition (MET). STAT3 functionally associates with MCL-1 in the mammalian breast cancer cell line MCF7 that overexpresses STAT3 and MCL-1, which leads to an increased rate of apoptosis and decreased cellular invasion, disrupting the EMT. Association of MCL-1 with STAT3 modulates the normal, antiapoptotic, activity of MCL-1, resulting in pro-apoptotic effects. Studying the impact of the association of STAT3 with MCL-1 on MET could lead to an enhanced understanding of pregnancy and infertility, and also metastatic tumors.

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Section: Discussionsupporting

confidence: 79%

STAT3 and MCL-1 associate to cause a mesenchymal epithelial transition

Renjini

Titus

Narayan

et al. 2014

Journal of Cell Science

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“…Increasing evidence suggests that the EMT of endometrial epithelial cells contributes to the establishment of endometriotic lesions 29, 30. In contrast, recent studies have provided compelling evidence that decidualization is associated with the MET of HEuESCs 31, 32. The authors demonstrated that decidualized stimulation down‐regulated N‐cadherin expression and up‐regulated E‐cadherin expression in the HEuESCs.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of microRNA‐542‐3p attenuates the differentiating capacity of endometriotic stromal cells

Sultana

Kajihara

Mizuno

et al. 2017

Reprod Medicine & Biology

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AimEndometriosis is defined as the presence of endometrial glandular and stromal cells outside of the uterine cavity. A previous study reported that microRNA (miR)‐542‐3p plays a critical role in eutopic endometrial decidualization. This study aims to clarify the potential role of miR‐542‐3p and the target gene, IGFBP‐1 (insulin‐like growth factor‐binding protein 1), in the impairment of the decidualizing capacity of human ectopic endometrial stromal cells (HEcESCs).MethodsIn vitro analysis of primary undifferentiated and decidualizing human eutopic endometrial stromal cells (HEuESCs) and HEcESCs was conducted. The primary HEuESCs or HEcESCs were expanded in culture and decidualized with 8‐bromo‐cyclic adenosine monophosphate (8‐bromo‐cAMP) and medroxyprogesterone acetate (MPA).ResultsThe morphological and biological differentiating capacities of the HEcESCs were markedly impaired. In contrast to the HEuESCs, the HEcESCs that were treated with the decidual stimulus retained the mesenchymal phenotype and capacity for migration. The down‐regulation of miR‐542‐3p in the HEcESCs treatment with 8‐bromo‐cAMP and MPA was much weaker than that of the HEuESCs. High expression of miR‐542‐3p led to a significant decrease in the expression of IGFBP1 in the HEcESCs.ConclusionImpairment of the differentiating capacity by the overexpression of miR‐542‐3p could influence the capacity for migration and invasion of endometriotic cells in an ectopic environment.

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“…Some years ago, on an animal model, it was observed that E-cadherin knockout mice were infertile due to defects in implantation and decidualization processes (28). More recently, an in vitro study, showed that decidualization is characterized by the down-regulation of some mesenchimal markers (such as SNAIL, vimentin) and the upregulation (such as E-cadherin, cytocheratin) of some epithelial markers in uterine stromal cells (27).…”

Section: Mechanisms Regulating the Embryo Endometrial Cross-talkmentioning

confidence: 99%

“…Moreover, it was observed that endometrial cells adhesion to a trophoblast cell line resulted improved after being exposed to implanted blastocyst medium compared with unexposed control (15). EMT process, activated by endocrine and paracrine effects of steroids hormones, and by soluble factors released by blastocyst and immune cells, promotes the endometrium decidualization, a process characterized by the differentiation of fibroblast-like endometrial stromal cells into epithelial like cells (26,27). Some years ago, on an animal model, it was observed that E-cadherin knockout mice were infertile due to defects in implantation and decidualization processes (28).…”

Section: Mechanisms Regulating the Embryo Endometrial Cross-talkmentioning

confidence: 99%

Periostin and implantation: a new biomarker of embryo-endometrial cross talk

Cello¹

2015

CCE

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SummaryEmbryo-endometrium cross-talk represents the main limiting factor for a good implantation and pregnancy. At the time of implantation the interaction between blastocyst and endometrium, mediated by sex steroids hormones, immune cells and related soluble factors, induces significant modification in the superficial profile of extracellular matrix (ECM) proteins in both endometrium and blastocyst. More recently, it has been shown that also periostin (POSTN), a secreted ECM protein and a key element in metastatic processes plays an important role in the regulation of the embryo-endometrium cross-talk. It was observed that serum levels and tissue expression of POSTN may predict endometrial receptivity and pregnancy outcome implantation. Furthermore, ongoing data show a relationship between follicular fluid POSTN concentrations and embryo quality. Although a clinical validation it's required, preliminary results showed that, besides to the morphological, morphokinetic and genetic criteria, POSTN could be an easy non invasive biomarker to evaluate blastocyst quality and chance to obtain an adequate implantation. In this review we describe the main mechanisms by which POSTN may play its role in the regulation of embryo endometrium cross-talk.

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The Mesenchymal—Epithelial Transition During In Vitro Decidualization

Cited by 68 publications

References 27 publications

STAT3 and MCL-1 associate to cause a mesenchymal epithelial transition

STAT3 and MCL-1 associate to cause a mesenchymal epithelial transition

Overexpression of microRNA‐542‐3p attenuates the differentiating capacity of endometriotic stromal cells

Periostin and implantation: a new biomarker of embryo-endometrial cross talk

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