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Establishing 3D Endometrial Organoids from the Mouse Uterus
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MAML1: a coregulator that alters endometrial epithelial cell adhesive capacity
Sadaf Zafir1,2, Wei Zhou1,2, Ellen Menkhorst1,2
1Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, Victoria, 3010, Australia.
Fertility Research and Practice
|March 28, 2021
Summary
Mastermind Like Transcriptional Coactivator 1 (MAML1) is crucial for endometrial receptivity, enhancing embryo implantation. Its knockdown reduces endometrial adhesive capacity, impacting key receptivity markers.
Area of Science:
- Reproductive biology
- Cell signaling
- Molecular endocrinology
Background:
- Endometrial receptivity is vital for embryo implantation, occurring during the mid-secretory phase.
- Dysregulation of Notch signaling components is observed in infertile women's endometria.
- Mastermind Like Transcriptional Coactivator 1 (MAML1) is a key Notch pathway coactivator.
Purpose of the Study:
- To investigate the role of MAML1 in regulating human endometrial receptivity.
- To determine MAML1's impact on endometrial epithelial cell adhesion to trophoblast cells.
Main Methods:
- Immunohistochemistry to assess MAML1 expression in human endometrium.
- MAML1 knockdown in Ishikawa cells to evaluate effects on adhesion to HTR8/SVneo spheroids.
- qPCR to analyze receptivity markers and pathway members post-MAML1 knockdown.
Main Results:
- MAML1 expression increased in the mid-secretory phase, localized to luminal epithelium.
- MAML1 knockdown significantly reduced Ishikawa cell adhesion to trophoblast spheroids.
- MAML1 knockdown altered expression of receptivity markers (SPP1, DPP4) and ANKRD1, independent of hormone receptors.
Conclusions:
- MAML1 plays a significant role in regulating endometrial adhesive capacity.
- MAML1 may facilitate embryo attachment, potentially via the Notch signaling pathway.
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