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Endometriotic lesions exert distinct metabolic activity compared to paired eutopic endometrium at a single-cell level

ABSTRACT: Eutopic endometrium (EuE) and endometriotic peritoneal lesions (ectopic endometrium, EcE) are heterogenous tissues according to the recent scRNA studies. We aimed to explore metabolic profile of cell populations in paired samples of EuE and EcE from four women with endometriosis. We found changes in the regulation of progesterone and estradiol signaling pathways in perivascular, stromal and endothelial cells of EcE compared to EuE, which might have a direct effect on cellular metabolism and contribute to cell proliferation and angiogenesis. The metabolic pathways were differentially regulated in perivascular, stromal and endothelial clusters, and metabolic pathway activity change between EcE and EuE was the highest for AMPK, HIF-1, glutathione metabolism, OXPHOS, and glycolysis/ gluconeogenesis. Remarkably, we identified co-activation of glycolysis and OXPHOS in perivascular and stromal cells of EcE compared to EuE. Previous studies reported a Warburg-like effect in endometriosis with a high use of glycolysis pathway over oxidative metabolism. Our observations might suggest the employment of both OXPHOS and glycolysis to meet the energy demands of proliferating cells in endometriotic lesions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE247695 | GEO | 2024/07/21

REPOSITORIES: GEO

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Project description:The pathophysiology of endometriotic lesion development remains unclear but involves a complex interaction between ectopic endometrium and host peritoneal tissues. We hypothesised that disruption of this interaction was likely to suppress endometriotic lesion formation. We hoped to delineate the molecular and cellular dialogue between ectopic human endometrium and peritoneal tissues in nude mice, as a first step towards testing this hypothesis. Human endometrium was xenografted into nude mice and the resulting lesions were analysed using microarrays. A novel technique was developed that unambiguously determined whether RNA transcripts identified by the microarray analyses originated from human cells (endometrium) or mouse cells (stroma). Four key pathways (ubiquitin/proteosome, inflammation, tissue remodelling/repair and ras-mediated oncogenesis) were revealed, that demonstrated communication between host stromal cells and ectopic endometrium. Morphometric analysis of nude mouse lesions confirmed that necrosis, inflammation, healing and repair and cell proliferation occurred during xenograft development. These processes were entirely consistent with the molecular networks revealed by the microarray data. The transcripts detected in the xenografts overlapped with transcripts differentially expressed in a comparison between paired eutopic and ectopic endometrium from human endometriotic patients. For the first time components of the interaction between ectopic endometrium and peritoneal stromal tissues have been revealed in ectopic endometrial lesions. Targeted disruption of this dialogue is likely to disrupt endometriotic tissue formation and may prove to be an effective therapeutic strategy for endometriosis. Experiment Overall Design: Xenografts of human endometrium in nude mice hybridised to both human and mouse specific genechips. 2 biological replicates, at 3 time points. Control human endometrium and mouse pertioneum were hybridised to both human and mouse genechips

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Endometriotic lesions exert distinct metabolic activity compared to paired eutopic endometrium at a single-cell level

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