Single-cell transcriptomic analysis of eutopic endometrium and ectopic lesions of adenomyosis
نویسندگان
چکیده
Abstract Background Adenomyosis (AM) is a common benign chronic gynaecological disorder; however, the precise pathogenesis of adenomyosis still poorly understood. Single-cell RNA sequencing (scRNA-seq) can uncover rare subpopulations, explore genetic and functional heterogeneity, reveal uniqueness each cell. It provides us new approach to biological issues from more detailed microscopic perspective. Here, we utilize this revolutionary technology identify changes gene expression patterns between ectopic lesions eutopic endometrium at single-cell level potential novel AM. Methods A control (sample with leiomyoma excluding endometrial disorders, n = 1), lesion (from patient adenomyosis, 1) samples were analysed by scRNA-seq, additional (n 3) used confirm colocalization vasculogenic mimicry (VM) formation. Protein was visualized immunofluorescence, CD34-periodic acid-Schiff (PAS) double staining assess formation VM. Results The scRNA-seq results suggest that cancer-, cell motility- inflammation- (CMI) associated terms, proliferation angiogenesis play important roles in progression Moreover, EPCAM PECAM1 increased significantly group (P < 0.05), subpopulation high copy number variation (CNV) levels possessing tumour-like features existed sample, VNN1- EPCAM-positive subcluster displayed active motility epithelial cells. Furthermore, during transformation cells endothelial cells, observed significant accumulation VM (positively stained PAS but not CD34, P 0.05) lesions. Conclusions In present study, our support theory derived invasion migration endometrium. CNV tumour-associated characteristics identified. epithelial-endothelial transition (EET) tumours, latter which facilitates blood supply plays an role maintaining growth, also confirmed occur These indicated inhibition EET may be strategy for AM management.
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ژورنال
عنوان ژورنال: Cell & Bioscience
سال: 2021
ISSN: ['2045-3701']
DOI: https://doi.org/10.1186/s13578-021-00562-z