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Войти в исследования Integrative biology : quantitative biosciences from nano to macro · 2026
Characterization of decidual natural killer cells cell heterogeneity and dynamic evolution in recurrent miscarriage based on single cell RNA-seq analysis.
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Fu Binbin, Wang Huijing
Аннотация
PURPOSE: This study used scRNA-seq to explore the underlying mechanisms of decidual natural killer cells affecting recurrent miscarriage (RM).
METHODS: We obtained the GSE214607 scRNA-seq dataset from Gene Expression Omnibus (GEO) database, containing data from 5 normal and 3 RM pregnancy samples. The 'Seurat' and 'Harmony' R package was used for the scRNA-seq analysis. Differentially expressed genes among cell subpopulations were identified using FindAllMarkers function, and the 'Monocle2' package was employed to construct pseudo-time trajectories. Finally, the 'CellChat' package was used to analyze ligand-receptor interactions between cells.
RESULTS: Our analysis revealed altered immune cell composition in RM, with reduced decidual NK (dNK), decidual stromal, and epithelial glandular cells but increased Mono/Macro proportions. Two dNK subclusters were identified: PAEP-high (linked to growth factor signaling) and LGALS1-high (involved in glycolysis and platelet function). Despite similar subcluster frequencies, RM samples showed elevated interferon response genes (e.g. IFITM1, ISG15) and diminished migration/activation signals. Pseudo-time analysis highlighted progressive gene expression changes during RM. CellChat revealed reduced Vascular Endothelial Growth Factor (VEGF) signaling, indicating impaired angiogenesis, and enhanced TNF, MHC-II, and FAS/FASL interactions, suggesting increased inflammation and trophoblast apoptosis. These findings implicate dNK dysfunction in RM and suggest potential therapeutic targets.
CONCLUSIONS: Our findings demonstrate dNK cell dysfunction in RM, marked by heightened interferon signaling and aberrant crosstalk with trophoblasts. Integrative analysis of public transcriptomic data suggests that dNK cell-directed interventions represent a putative therapeutic avenue for RM. Insight RM linked to decidual immune imbalance with reduced dNK and increased monocytes/macrophages. Two dNK subclusters (PAEP-high, LGALS1-high) with specific gene expression pattern in RM. RM shows impaired angiogenesis, inflammation, and trophoblast apoptosis in dNK cell-mediated signaling pathways. Dysfunctional dNK cells drive RM, revealing potential therapeutic targets for treatment.
METHODS: We obtained the GSE214607 scRNA-seq dataset from Gene Expression Omnibus (GEO) database, containing data from 5 normal and 3 RM pregnancy samples. The 'Seurat' and 'Harmony' R package was used for the scRNA-seq analysis. Differentially expressed genes among cell subpopulations were identified using FindAllMarkers function, and the 'Monocle2' package was employed to construct pseudo-time trajectories. Finally, the 'CellChat' package was used to analyze ligand-receptor interactions between cells.
RESULTS: Our analysis revealed altered immune cell composition in RM, with reduced decidual NK (dNK), decidual stromal, and epithelial glandular cells but increased Mono/Macro proportions. Two dNK subclusters were identified: PAEP-high (linked to growth factor signaling) and LGALS1-high (involved in glycolysis and platelet function). Despite similar subcluster frequencies, RM samples showed elevated interferon response genes (e.g. IFITM1, ISG15) and diminished migration/activation signals. Pseudo-time analysis highlighted progressive gene expression changes during RM. CellChat revealed reduced Vascular Endothelial Growth Factor (VEGF) signaling, indicating impaired angiogenesis, and enhanced TNF, MHC-II, and FAS/FASL interactions, suggesting increased inflammation and trophoblast apoptosis. These findings implicate dNK dysfunction in RM and suggest potential therapeutic targets.
CONCLUSIONS: Our findings demonstrate dNK cell dysfunction in RM, marked by heightened interferon signaling and aberrant crosstalk with trophoblasts. Integrative analysis of public transcriptomic data suggests that dNK cell-directed interventions represent a putative therapeutic avenue for RM. Insight RM linked to decidual immune imbalance with reduced dNK and increased monocytes/macrophages. Two dNK subclusters (PAEP-high, LGALS1-high) with specific gene expression pattern in RM. RM shows impaired angiogenesis, inflammation, and trophoblast apoptosis in dNK cell-mediated signaling pathways. Dysfunctional dNK cells drive RM, revealing potential therapeutic targets for treatment.