Relevance of Wnt10b and activation of β‐catenin/<scp>GCM</scp>a/syncytin‐1 pathway in BeWo cell fusion

Malhotra, Sudha Saryu; Banerjee, Priyanka; Chaudhary, Piyush; Pal, Rahul; Gupta, Satish Kumar

doi:10.1111/aji.12676

Cited by 13 publications

(11 citation statements)

References 29 publications

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“…Also, it has been reported that a feedback loop involving Gcm1 and Frizzled regulates trophoblast differentiation and chorionic branching morphogenesis 8 . Additionally, Wnt10b is involved in the activation of β-catenin/GCM1 pathway during the process of BeWo cell fusion after forskolin/hCG treatment 9 . These findings suggested that Gcm1 may be linked with Wnt signaling pathway, which can affect its activity to control cell fate.…”

Section: Introductionmentioning

confidence: 99%

Aberrant Gcm1 expression mediates Wnt/β-catenin pathway activation in folate deficiency involved in neural tube defects

Xie

Gao

et al. 2021

Cell Death Dis

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Wnt signaling plays a major role in early neural development. An aberrant activation in Wnt/β-catenin pathway causes defective anteroposterior patterning, which results in neural tube closure defects (NTDs). Changes in folate metabolism may participate in early embryo fate determination. We have identified that folate deficiency activated Wnt/β-catenin pathway by upregulating a chorion-specific transcription factor Gcm1. Specifically, folate deficiency promoted formation of the Gcm1/β-catenin/T-cell factor (TCF4) complex formation to regulate the Wnt targeted gene transactivation through Wnt-responsive elements. Moreover, the transcription factor Nanog upregulated Gcm1 transcription in mESCs under folate deficiency. Lastly, in NTDs mouse models and low-folate NTDs human brain samples, Gcm1 and Wnt/β-catenin targeted genes related to neural tube closure are specifically overexpressed. These results indicated that low-folate level promoted Wnt/β-catenin signaling via activating Gcm1, and thus leaded into aberrant vertebrate neural development.

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Section: Introductionmentioning

confidence: 99%

Aberrant Gcm1 expression mediates Wnt/β-catenin pathway activation in folate deficiency involved in neural tube defects

Xie

Gao

et al. 2021

Cell Death Dis

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“…Success of pregnancy relies on the differentiation, proliferation, and invasion of placental trophoblast cells during early pregnancy [26,27] . The dysfunction of trophoblast may lead to severe complications threatening both the mother and the developing fetus and resulting in economic losses.…”

Section: Discussionmentioning

confidence: 99%

Placental Trophoblast Derived Exosomes Regulate Endometrial Epithelial Receptivity in Dairy Cows During Pregnancy

Zhang

et al. 2021

Preprint

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Background Inadequate feto-maternal interaction will directly lead to the failures of pregnancy and bring serious damage to dairy cows. Exosomes are widely involved in endometrial matrix remodeling, immune function changes, placental development, and other processes of embryo implantation and pregnancy of dairy cows. However, the role of placental trophoblast cells derived exosomes is still unclear in regulating the receptivity of endometrial cells and facilitating the interaction between mother and fetus. Methods In this study, bovine trophoblast cells (BTCs) were obtained from bovine placenta and immortalized through the transfection of telomerase reverse transcriptase (TERT) gene. After that, the effect of trophoblast derived exosomes (TDEs) on endometrial receptivity in endometrial epithelial cells (EECs) was detected and the mechanism explored that TDEs and their proteins participated in feto-maternal interaction during bovine pregnancy. EECs were co-cultured with the exosomes derived from progesterone (P4) and treated with BTCs. Results Immortalized BTCs still possessed the basic and key properties of primary BTCs without showing a neoplastic transformation sign. Exosomes derived from P4 and treated with BTCs enhanced the expression of endometrial receptivity factors in EECs by changing the extracellular environment, metabolism and redox balance in EECs with proteome alignment, compared with those untreated according to the DIA quantitation analysis. Conclusions Our study found that trophoblast derived exosomal proteins are one of the most critical elements in feto-maternal interaction and their changes act as a key signal in altering endometrial receptivity and provided a potential target for improving fertility.

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“…BeWo cells (0.1 × 10 6 /well), seeded 24 h prior in 6‐well cell culture plates, were transfected with optimized concentration of either miR‐27b‐5p mimic (50 nM) & mimic control (50 nM; GE Dharmacon™), or WNT2B siRNA, HSD3β1 siRNA & control siRNA (40 pmol; Qiagen) using lipofectamine™ RNAiMAX transfection reagent (LifeTechnologies) and Opti‐MEM ® (Gibco®) essentially as described previously 18 . In addition, BeWo cells were also co‐transfected with miR‐27b‐5p mimic and optimized concentration of either mammalian HSD3β1 (300 ng/ml; Sino Biological) or WNT2B (500 ng/ml; Sino Biological) expression vector to see, if overexpression of HSD3β1/WNT2B can rescue the effect of miR‐27b‐5p mimic on forskolin‐mediated BeWo cell fusion.…”

Section: Methodsmentioning

confidence: 99%

“…Qiagen) using lipofectamine™ RNAiMAX transfection reagent (LifeTechnologies) and Opti-MEM ® (Gibco®) essentially as described previously. 18 In addition, BeWo cells were also co-transfected with miR-27b-5p mimic and optimized concentration of either mammalian HSD3β1 (300 ng/ml; Sino Biological) or WNT2B (500 ng/ml; Sino Biological) expression vector to see, if overexpression of HSD3β1/ WNT2B can rescue the effect of miR-27b-5p mimic on forskolinmediated BeWo cell fusion. After 48 h of transfection, cells were processed for cell viability, fusion, qRT-PCR, and Western blotting.…”

Section: Bioinformatics Analysis Of Mir-27b-5p Targetsmentioning

confidence: 99%

miR‐27b‐5p inhibits BeWo cells fusion by regulating WNT2B and enzyme involved in progesterone synthesis

Verma

Mishra

Malik

et al. 2021

American J Rep Immunol

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Problem:The miRNAs show placenta-specific expression patterns, which alter during pregnancy-related complications. In present study, the role of miR-27b-5p during forskolin-mediated BeWo cells fusion has been investigated. Method ofStudy: The fusion of BeWo cells in response to forskolin treatment (25 µM) was studied by desmoplakin I+II staining. Expression profile of miR-27b-5p by qRT-PCR and its targets HSD3β1 and WNT2B by qRT-PCR and in Western blot were studied. The effect of overexpression of miR-27b-5p and silencing of HSD3β1 & WNT2B by siRNA on forskolin-mediated BeWo cells fusion and secretion of hCG and progesterone by ELISA was investigated. Results: Time-dependent down-regulation in the expression of miR-27b-5p in forskolin-treated BeWo cells has been confirmed by qRT-PCR. Overexpression of miR-27b-5p significantly inhibits forskolin-mediated BeWo cells fusion as well as hCG & progesterone secretion. HSD3β1 and WNT2B were identified as targets of miR-27b-5p and are up-regulated in forskolin-treated BeWo cells. Overexpression of miR-27b-5p in BeWo cells downregulates their expression. Further, luciferase reporter assay revealed that miR-27b-5p directly target expression of both HSD3β1 and WNT2B. Silencing of both HSD3β1 and WNT2B leads to a significant reduction in forskolin-mediated BeWo cells fusion with concomitant decrease in the secretion of progesterone or/and hCG. Decrease in forskolin-mediated cells fusion observed in miR-27b-5p mimic transfected BeWo cells could be rescued by the overexpression of both HSD3β1 and WNT2B. Conclusion: These observations suggest that reduced miR-27b-5p in forskolin-treated BeWo cells leads to increased secretion of progesterone and hCG due to loss of repressional control on HSD3β1 and WNT2B.

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Relevance of Wnt10b and activation of β‐catenin/GCMa/syncytin‐1 pathway in BeWo cell fusion

Abstract: Wnt10b is involved in forskolin/hCG-mediated BeWo cell fusion via β-catenin/GCMa/syncytin pathway, which may also involve activation of PKA.

Cited by 13 publications

References 29 publications

Aberrant Gcm1 expression mediates Wnt/β-catenin pathway activation in folate deficiency involved in neural tube defects

Aberrant Gcm1 expression mediates Wnt/β-catenin pathway activation in folate deficiency involved in neural tube defects

Placental Trophoblast Derived Exosomes Regulate Endometrial Epithelial Receptivity in Dairy Cows During Pregnancy

miR‐27b‐5p inhibits BeWo cells fusion by regulating WNT2B and enzyme involved in progesterone synthesis

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