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Metabolic reprogramming driven by impaired trophoblasts and decidual XCR1+PMN-MDSCs crosstalk controls adverse outcomes in advanced maternal age [CUT&Tag]

ABSTRACT: Decidual polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are crucial for maternal–fetal stability and accumulate to support fetal development. Although advanced maternal age (AMA) increases the risk of adverse outcomes, the regulatory role and mechanism of decidual PMN-MDSCs in these outcomes remain unclear. Herein, the XCL1–XCR1 interaction mediated specific crosstalk between trophoblast cells and decidual PMN-MDSCs in both humans and mice. Single-cell sequencing identified a decidual PMN-MDSCs subset highly expressing XCR1 markedly reduced in AMA. Impaired XCL1-stimulated decidual XCR1+PMN-MDSCs delayed fetal growth in AMA and Xcr1-/- pregnant mice. Perinatal XCL1 supplementation and oltipraz treatment rescued these functions by activating decidual XCR1+PMN-MDSCs in AMA mice, not Xcr1-/- pregnant mice. The XCL1–XCR1 axis induced FOXO1 nuclear localization, regulating oxidative phosphorylation-related targets and enabling metabolic processes. Hence, XCL1–XCR1 crosstalk between trophoblast cells and PMN-MDSCs is critical in driving metabolic reprogramming of decidual XCR1+PMN-MDSCs and controlling adverse outcomes caused by AMA.

ORGANISM(S): Mus musculus

PROVIDER: GSE288405 | GEO | 2026/04/08

REPOSITORIES: GEO

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Metabolic reprogramming driven by impaired trophoblasts and decidual XCR1+PMN-MDSCs crosstalk controls adverse outcomes in advanced maternal age [RNA-Seq]

Project description:Decidual polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are crucial for maternal–fetal stability and accumulate to support fetal development. Although advanced maternal age (AMA) increases the risk of adverse outcomes, the regulatory role and mechanism of decidual PMN-MDSCs in these outcomes remain unclear. Herein, the XCL1–XCR1 interaction mediated specific crosstalk between trophoblast cells and decidual PMN-MDSCs in both humans and mice. Single-cell sequencing identified a decidual PMN-MDSCs subset highly expressing XCR1 markedly reduced in AMA. Impaired XCL1-stimulated decidual XCR1+PMN-MDSCs delayed fetal growth in AMA and Xcr1-/- pregnant mice. Perinatal XCL1 supplementation and oltipraz treatment rescued these functions by activating decidual XCR1+PMN-MDSCs in AMA mice, not Xcr1-/- pregnant mice. The XCL1–XCR1 axis induced FOXO1 nuclear localization, regulating oxidative phosphorylation-related targets and enabling metabolic processes. Hence, XCL1–XCR1 crosstalk between trophoblast cells and PMN-MDSCs is critical in driving metabolic reprogramming of decidual XCR1+PMN-MDSCs and controlling adverse outcomes caused by AMA.

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