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Related Experiment Video

Updated: May 2, 2026

Isolation and Profiling of Human Primary Mesenteric Arterial Endothelial Cells at the Transcriptome Level
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Spatial and single-cell transcriptomics landscape of adenomyosis.

Xing Yang1, Chunjie Li2, Junxian He3

  • 1Reproductive Medicine Center, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; GuangDong Engineering Technology Research Center of Fertility Preservation, Guangzhou, China; Department of Obstetrics and Gynecology, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Journal of Advanced Research
|December 28, 2025
PubMed
Summary

This study reveals ciliated epithelial cells and immune-angiogenic crosstalk in adenomyosis pathogenesis. Gonadotropin-releasing hormone agonists (GnRHa) normalize immune cells and restore interactions, offering therapeutic insights.

Keywords:
AdenomyosisCiliated cellGnRHa treatmentSingle-cell transcriptomicsSpatial transcriptomics

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Area of Science:

  • Gynecological disorders
  • Reproductive medicine
  • Cellular and molecular mechanisms

Background:

  • Adenomyosis is a common gynecological disorder with poorly understood causes.
  • Gonadotropin-releasing hormone agonists (GnRHa) are used to treat adenomyosis, but their cellular effects are unclear.

Purpose of the Study:

  • To profile adenomyosis using single-cell and spatial transcriptomics.
  • To evaluate the effects of GnRHa treatment on cellular populations in adenomyosis.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (Geo-seq) were used.
  • 15 participants (11 adenomyosis, 4 controls) were profiled.
  • Immunofluorescence and immunohistochemistry validated findings.

Main Results:

  • Ectopic endometrial glands in adenomyosis showed enrichment of ciliated epithelial cells.
  • Immune-inflammatory signatures (CD4+ T cells, LYVE1+ macrophages) were prominent in untreated adenomyosis.
  • GnRHa treatment partially mitigated inflammation and angiogenesis; mast cells were concentrated in the junctional zone.

Conclusions:

  • Findings support the invagination theory, implicating ciliated cells and immune-angiogenic crosstalk.
  • GnRHa normalizes immune cell composition and epithelial-stromal interactions.
  • Novel mechanistic insights into GnRHa's therapeutic action were provided.