A Galectin-9–Driven CD11c high Decidual Macrophage Subset Suppresses Uterine Vascular Remodeling in Preeclampsia
Authors' conclusion
These findings highlight a key role of a distinct perivascular inflammatory CD11chigh dMφ subpopulation in the pathogenesis of preeclampsia. CD11chigh dMφ activated by increased galectin-9 from trophoblasts suppresses uterine spiral artery remodeling, contributing to preeclampsia.
Study context
- Population
- Patients with preeclampsia and preeclampsia mouse models
Methodological detailssingle-cell RNA sequencing, spatial transcriptomics, conditional knockout mice, retrospective cohort
- Single-cell RNA sequencing
- Spatial transcriptomics
- Conditional knockout mice
- Retrospective cohort
Main finding
As reported in the abstract
- Distinct CD11chigh dMφ subset inhibits spiral artery remodeling in preeclampsia
- Proinflammatory CD11chigh dMφ show perivascular enrichment in decidua from patients with preeclampsia
- Trophoblast-derived galectin-9 activates CD11chigh dMφ via CD44 binding to suppress spiral artery remodeling
- Placental and plasma galectin-9 elevated in 3 independent preeclampsia mouse models
- Galectin-9 administration in mice induces preeclampsia-like phenotypes with increased CD11chigh dMφ and defective spiral arteries; galectin-9 blockade or macrophage-specific CD44 deletion prevents them
- Increased circulating galectin-9 in the first trimester and at 16 to 20 gestational weeks predicts subsequent preeclampsia onset
Original publication
A Galectin-9–Driven CD11c high Decidual Macrophage Subset Suppresses Uterine Vascular Remodeling in Preeclampsia. Circulation. Published 5 February 2024. doi:10.
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