Exploration of the pathological mechanism of endometriosis in rats using high-throughput sequencing

Fu-Rui Miao, LI Zhen-juan, Muyue Li, Yu-Shan Fan
2019 · doi:10.21203/rs.2.16343/v1 · W4214594579
preprint OA: green CC0
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study used high-throughput sequencing in a rat model of endometriosis to identify differentially expressed genes and enriched pathways, revealing inflammation and phagocyte involvement in ectopic endometrial lesion development.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This preprint used a rat model of endometriosis, comparing an endometriosis (EMs) model group, a sham operation group, and a drug treatment group given gestrinone, then performed uterine tissue RNA sequencing with quality control and differential expression analysis. High-throughput sequencing produced acceptable read quality and mapping rates, and the drug treatment group showed 440 differentially expressed genes versus sham, while the drug treatment and sham each differed from the model group (382 and 503 DEGs, respectively). Differentially expressed genes were enriched in immune/inflammatory and cytoskeletal or adhesion-related pathways (including phagosome, NK cell-mediated cytotoxicity, cytokine–cytokine receptor interaction, and JAK/STAT signaling), and the authors highlighted genes related to the vascular endothelial growth factor pathway (ENSRNOG00000023079 and ENSRNOG00000012175). A key limitation explicitly noted by the preprint is that it is based on a small number of rats (nine total) and does not claim journal peer review; This paper is centrally about endometriosis — it uses high-throughput sequencing in rats to probe inflammatory, phagocyte-related mechanisms and VEGF-associated gene changes in EMs lesions.

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Abstract

Abstract Background : This study aimed to explore the pathological mechanism of endometriosis (EMs) in rats by high-throughput sequencing. Methods : Rat EMs model, sham operation group and drug treatment group were established. Uterine tissue was collected for construction of sequencing library and high-throughput sequencing. Data quality was examined. KEGG pathway enrichment analysis was carried out. Results : Percentages of both high-quality sequence Reads and high-quality sequence bases accounted for more than 98%, suggesting that the data quality was acceptable. Total sequences mapped to reference genome (Total Mapped) accounted for more than 90% of total sequences used for mapping (Clean Reads), suggesting that the mapping results of the sequencing data were acceptable. There were 440 differentially expressed genes (DEGs) in the drug treatment group compared with the sham operation group, 382 DEGs in the drug treatment group compared with the model group, and 503 DEGs in the sham operation group compared with the model group. We screened genes ENSRNOG00000023079 and ENSRNOG00000012175 related to vascular endothelial growth factor pathway. The DEGs were mainly enriched in the signaling pathways such as phagosome, natural killer cell mediated cytotoxicity, Janus kinase-signal transducers and activators of transcription signaling pathway, hematopoietic cell lineage, cytokine-cytokine receptor interaction, regulation of actin cytoskeleton and extracellular matrix-receptor interaction. Conclusions : EMs might begin with the inflammatory response of the ectopic endometrium. Phagocytes played a key role in this process. The ectopic endometrium adhered to the abdominal wall with the help of the inflammation reaction, generated blood vessels, and finally transformed into growing lesions.

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Condition tags

endometriosis

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References (14)

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