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Oct 01, 2024;17 (10):

RNA sequencing reveals molecular mechanisms of endometriosis lesion development in mice.

Kavita Panir, John E Schjenken, James Breen, Hon Yeung Chan, Erin Greaves, Sarah A Robertson, M Louise Hull
Author Information
  1. Kavita Panir: Robinson Research Institute and School of Biomedicine, The University of Adelaide, Adelaide, SA 5006, Australia. ORCID
  2. John E Schjenken: Robinson Research Institute and School of Biomedicine, The University of Adelaide, Adelaide, SA 5006, Australia. ORCID
  3. James Breen: Robinson Research Institute and School of Biomedicine, The University of Adelaide, Adelaide, SA 5006, Australia. ORCID
  4. Hon Yeung Chan: Robinson Research Institute and School of Biomedicine, The University of Adelaide, Adelaide, SA 5006, Australia. ORCID
  5. Erin Greaves: Centre for Early Life, Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK. ORCID
  6. Sarah A Robertson: Robinson Research Institute and School of Biomedicine, The University of Adelaide, Adelaide, SA 5006, Australia. ORCID
  7. M Louise Hull: Robinson Research Institute and School of Biomedicine, The University of Adelaide, Adelaide, SA 5006, Australia. ORCID
PMID: 39385609 DOI: 10.1242/dmm.050566

Abstract

Understanding of molecular mechanisms contributing to the pathophysiology of endometriosis, and upstream drivers of lesion formation, remains limited. Using a C57Bl/6 mouse model in which decidualized endometrial tissue is injected subcutaneously in the abdomen of recipient mice, we generated a comprehensive profile of gene expression in decidualized endometrial tissue (n=4), and in endometriosis-like lesions at Day 7 (n=4) and Day 14 (n=4) of formation. High-throughput mRNA sequencing allowed identification of genes and pathways involved in the initiation and progression of endometriosis-like lesions. We observed distinct patterns of gene expression with substantial differences between the lesions and the decidualized endometrium that remained stable across the two lesion timepoints, and showed similarity to transcriptional changes implicated in human endometriosis lesion formation. Pathway enrichment analysis revealed several immune and inflammatory response-associated canonical pathways, multiple potential upstream regulators, and involvement of genes not previously implicated in endometriosis pathogenesis, including IRF2BP2 and ZBTB10, suggesting novel roles in disease progression. Collectively, the provided data will be a useful resource to inform research on the molecular mechanisms contributing to endometriosis-like lesion development in this mouse model.

Keywords

Endometriosis Immune regulation Mouse model RNA Sequencing

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Grants

  1. /Australian Government Research Training Program Scholarship
  2. /Allan and Joyce Ballantyne Medical and Surgical Education and Research Trust Grant
  3. /Australian Government
  4. /University of Adelaide

MeSH Term

Endometriosis
Animals
Female
Mice, Inbred C57BL
Sequence Analysis, RNA
Disease Models, Animal
Mice
Endometrium
Gene Expression Regulation
Gene Expression Profiling
Transcriptome
Humans
Journal Article
Article has an altmetric score of 2

Word Cloud

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