ArticleMolecular endocrinology (Baltimore, Md.)2011
Down-regulation of the histone methyltransferase EZH2 contributes to the epigenetic programming of decidualizing human endometrial stromal cells.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 84 citations in OpenAlex.
- Mechanisms of Luoshi Neiyi prescription (LSNYP) in endometriosis: a network pharmacology and experimental study.Hereditas · 2026Article
- Understanding epigenetic regulation in the endometrium - lessons from mouse models with implantation defects.Epigenomics · 2025Review
- Endometrial aging is accompanied by H3K27ac and PGR loss.Nature aging · 2025Article
- Molecular Basis of Impaired Decidualization in the Eutopic Endometrium of Endometriosis Patients.Cells · 2025Review
- H3K27me3 timely dictates uterine epithelial transcriptome remodeling and thus transformation essential for normal embryo implantation.Cell death and differentiation · 2024Article
- Decreased NSD2 impairs stromal cell proliferation in human endometrium via reprogramming H3K36me2.Reproduction (Cambridge, England) · 2024Article
- Potential mechanism of Luoshi Neiyi prescription in endometriosis based on serum pharmacochemistry and network pharmacology.Frontiers in pharmacology · 2024Article
- Uterine-specificiScience · 2023Article
- CFP1 governs uterine epigenetic landscapes to intervene in progesterone responses for uterine physiology and suppression of endometriosis.Nature communications · 2023Article
- Dysregulated Gln-Glu-α-ketoglutarate axis impairs maternal decidualization and increases the risk of recurrent spontaneous miscarriage.Cell reports. Medicine · 2023Article
- Histone modifications in embryo implantation and placentation: insights from mouse models.Frontiers in endocrinology · 2023Review
- Role of EZH2 in Uterine Gland Development.International journal of molecular sciences · 2022Article
- Epigenetic Features in Uterine Leiomyosarcoma and Endometrial Stromal Sarcomas: An Overview of the Literature.Biomedicines · 2022Review
- Article
- Efficient cell chatting between embryo and uterus ensures embryo implantation†.Biology of reproduction · 2022Article
- JAZF1-SUZ12 dysregulates PRC2 function and gene expression during cell differentiation.Cell reports · 2022Article
- Role of inflammation in benign gynecologic disorders: from pathogenesis to novel therapies†.Biology of reproduction · 2021Review
- Menstrual Blood-Derived Endometrial Stem Cells' Impact for the Treatment Perspective of Female Infertility.International journal of molecular sciences · 2021Article
- The role of epigenetic mechanisms in the regulation of gene expression in the cyclical endometrium.Clinical epigenetics · 2021Review
- The Role of Decidual Subpopulations in Implantation, Menstruation and Miscarriage.Frontiers in reproductive health · 2021Review
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differentiation of human endometrial stromal cells (HESC) into decidual cells represents a highly coordinated process essential for embryo implantation. We show that decidualizing HESC down-regulate the histone methyltransferase enhancer of Zeste homolog 2 (EZH2), resulting in declining levels of trimethylation of histone 3 on lysine 27 (H3K27me3) at the proximal promoters of key decidual marker genes PRL and IGFBP1. Loss of H3K27me3 was associated with a reciprocal enrichment in acetylation of the same lysine residue, indicating active remodeling from repressive to transcriptionally permissive chromatin. Chromatin immunoprecipitation coupled with DNA microarray analysis demonstrated that decidualization triggers genome-wide changes in H3K27me3 distribution that only partly overlap those observed upon EZH2 knockdown in undifferentiated HESC. Gene ontology revealed that gain of the repressive H3K27me3 mark in response to decidualization and upon EZH2 knockdown in undifferentiated cells was enriched at the promoter regions of genes involved in transcriptional regulation and growth/cell proliferation, respectively. However, loss of the H3K27me3 mark (indicating increased chromatin accessibility) in decidualizing cells and upon EZH2 knockdown occurred at selective loci enriched for genes functionally implicated in responses to stimulus. In agreement, EZH2 knockdown in undifferentiated HESC was sufficient to augment the induction of decidual marker genes in response to cyclic AMP and progesterone signaling. Thus, loss of EZH2-dependent methyltransferase activity in the endometrium is integral to the process of chromatin remodeling that enables the transition from a proliferative to a decidual phenotype in response to differentiation cues.
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