ArticleCell proliferation2022
Glycomics reveal that ST6GAL1-mediated sialylation regulates uterine lumen closure during implantation.
Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Deficient extravillous trophoblast invasion caused by impaired sialylation-Siglec-7 interaction contributes to recurrent pregnancy loss.Cell death & disease · 2026Article
- Chemerin's Role in Endometrial Dysfunction: Insights From Transcriptomic Analysis.Journal of cellular and molecular medicine · 2025Article
- Unveiling sialoglycans' immune mastery in pregnancy and their intersection with tumor biology.Frontiers in immunology · 2024Review
- Lewis x-carrying O-glycans are candidate modulators for conceptus attachment in pigs†.Biology of reproduction · 2023Article
- Glycomics reveal that ST6GAL1-mediated sialylation regulates uterine lumen closure during implantation.Cell proliferation · 2022Article
- Analysis of carbohydrates and glycoconjugates by matrix-assisted laser desorption/ionization mass spectrometry: An update for 2021-2022.Mass spectrometry reviewsReview
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesImplantation failure is a major cause of prenatal mortality. The uterine lumen closure contributes to embryo adhesion to the uterus, but its underlying mechanisms are largely unknown. Our previous study has reported that endometrial fold extension can lead to uterine lumen closure in pigs. The objective of this study was to reveal molecular mechanisms of the uterine lumen closure by characterizing the molecular basis of the endometrial fold extension during implantation in pigs. MATERIALS AND
methodsUterine and endometrium tissues during implantation were collected in pigs. MALDI-TOF MS was used to characterize the N-glycomic profiles. Histochemistry, siRNA transfection, Western blotting, lectin immumoprecipitation, mass spectrometry and assays of wounding healing and cell aggregation were performed to investigate the molecular basis.
resultsWe observed that uterine luminal epithelium (LE) migrated collectively during endometrial fold extension. For the first time, we identified a large number of N-glycan compositions from endometrium during implantation using MALDI-TOF MS. Notably, the α2,6-linked sialic acid and ST6GAL1 were highly expressed in uterine LE when the endometrial folds extended greatly. Subsequently, the role of ST6GAL1-mediated 2,6-sialylation in collective epithelial migration was demonstrated. Finally, we found that ST6GAL1-mediated α2,6-sialylation of E-cadherin may participate in collective migration of uterine LE.
conclusionsThe study reveals a mechanism of uterine lumen closure by identifying that ST6GAL1-mediated α2,6-sialylation of cell adhesion molecules contributes to endometrial fold extension through regulating collective migration of uterine LE.
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