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

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.