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Updated: Jun 11, 2025
A Syngeneic Murine Model of Endometriosis using Naturally Cycling Mice
Published on: November 24, 2020
RNA sequencing reveals molecular mechanisms of endometriosis lesion development in mice
Kavita Panir1,2, John E Schjenken1,2,3,4, James Breen1,2,5,6
1Robinson Research Institute and School of Biomedicine, The University of Adelaide, Adelaide, SA 5006, Australia.
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.
Insights
This study reveals distinct gene expression patterns in endometriosis-like lesions, identifying novel genes like IRF2BP2 and ZBTB10. These findings offer insights into the molecular mechanisms driving endometriosis progression.
Area of Science:
- Reproductive biology
- Molecular pathology
- Genomics
Background:
- The molecular mechanisms and upstream drivers of endometriosis pathophysiology and lesion formation are not fully understood.
- Limited knowledge exists regarding the specific genetic and molecular changes during the early stages of endometriosis development.
Purpose of the Study:
- To comprehensively profile gene expression in an endometriosis mouse model to identify key molecular players and pathways involved in lesion initiation and progression.
- To uncover novel genes and regulatory mechanisms contributing to endometriosis pathogenesis.
Main Methods:
- Utilized a C57Bl/6 mouse model for endometriosis, involving subcutaneous injection of decidualized endometrial tissue.
- Performed high-throughput mRNA sequencing on decidualized endometrium and endometriosis-like lesions at Day 7 and Day 14.
- Conducted pathway enrichment analysis to identify involved biological processes and potential regulators.
Main Results:
- Observed distinct and stable gene expression patterns in endometriosis-like lesions compared to the decidualized endometrium across timepoints.
- Transcriptional changes in the mouse model showed similarity to those implicated in human endometriosis.
- Identified immune and inflammatory response pathways, potential upstream regulators, and novel genes such as IRF2BP2 and ZBTB10 involved in lesion development.
Conclusions:
- The study provides a valuable gene expression dataset for understanding endometriosis molecular mechanisms in a mouse model.
- Identified novel genes and pathways, including IRF2BP2 and ZBTB10, suggesting new therapeutic targets for endometriosis.
- The findings contribute to a deeper understanding of endometriosis pathophysiology and lesion formation.
