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Single-cell sequencing reveals a delicate molecular and cellular interaction during decidualization in humans

ABSTRACT: Proper decidualization is a critical determinant of pregnancy success. Deficiencies in decidualization are associated with a variety of pregnancy disorders, including female infertility, recurrent implantation failure, and miscarriage. However, the mechanism for triggering decidualization of human endometrium is largely unknown. Here we characterized the transcriptomes of four major cells in human endometrium and decidua at single-cell resolution. We discovered the dynamic change characteristics of six major stromal cells. More importantly, a dialogue between IGF1+ stromal cells and IGF1R+ stromal cells initiates endometrial decidualization under regulation of progesterone and estrogen, and IL1B+ stromal cells trigger the apoptosis of epithelial cells and functional remodeling during decidualization. We defined a unique AREG+ NK cell for accelerating decidualization by interacting with IGF1+ stromal cells, and observed that extravillous trophoblasts promote decidualization possibly by multiply pathways. Additionally, we developed a systematic repository of cell-cell communication for decidualization via the ligand-receptor complexes interactions. Our study provides deeper insights into the molecular and cellular characterizations during decidualization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE194219 | GEO | 2022/11/24

REPOSITORIES: GEO

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Project description:Uterine receptivity implies a dialogue between the hormonally primed maternal endometrium and the free-floating blastocyst. Endometrial stromal cells proliferate, avert apoptosis, and undergo decidualization in preparation for implantation; however, the molecular mechanisms that underlie differentiation into the decidual phenotype remain largely undefined. The Notch family of transmembrane receptors transduce extracellular signals responsible for cell survival, cell-to-cell communication, and trans-differentiation, all fundamental processes for decidualization and pregnancy. Using a murine artificial decidualization model, pharmacological inhibition of Notch signaling by gamma-secretase inhibition resulted in significantly decreased deciduoma. Furthermore, a progesterone receptor (PR)-Cre Notch1 bigenic (Notch1d/d) confirmed a Notch1-dependant hypomorphic decidual phenotype. Microarray and pathway analysis, following Notch1 ablation, demonstrated significantly altered signaling repertoire. Concomitantly, hierarchical clustering demonstrated Notch1-dependent differences in gene expression. Uteri deprived of Notch1 signaling demonstrated decreased cellular proliferation; namely, reduced proliferation-specific antigen, Ki67, altered p21, cdk6, and cyclinD activity, and increased apoptotic-profile, augmented cleaved caspase-3, Bad, and attenuated Bcl2. Demonstrated here, the pre-implantation uterus relies on Notch signaling to inhibit apoptosis of stromal fibroblasts and regulate cell cycle progression, which together promotes successful decidualization. In summary, Notch1 signaling modulates multiple signaling mechanisms crucial for decidualization and we provide greater perspective to the coordination of multiple signaling modalities required during decidualization RNA samples from 3-5 separate mice were extracted. All mRNA quantities were normalized against 18S gene expression. Gene expression levels were measured by real-time RT-PCR SYBR Green analysis using the ABI Prism 7700 Sequence Detector System according to manufacturer’s instructions (Applied Biosystems).

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Single-cell sequencing reveals a delicate molecular and cellular interaction during decidualization in humans

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