Mesenchymal-to-epithelial transition of perivascular cells contributes to endometrial re-epithelialization

Shu-Yun Li, Sarah Whiteside, Bo Li, Xiaofei Sun () and Tony DeFalco ()
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Shu-Yun Li: Cincinnati Children’s Hospital Medical Center, Reproductive Sciences Center, Division of Developmental Biology
Sarah Whiteside: Cincinnati Children’s Hospital Medical Center, Reproductive Sciences Center, Division of Developmental Biology
Bo Li: Cincinnati Children’s Hospital Medical Center, Reproductive Sciences Center, Division of Developmental Biology
Xiaofei Sun: Cincinnati Children’s Hospital Medical Center, Reproductive Sciences Center, Division of Developmental Biology
Tony DeFalco: Cincinnati Children’s Hospital Medical Center, Reproductive Sciences Center, Division of Developmental Biology

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract Endometrial regeneration is essential for reproductive cycles and pregnancies, allowing the endometrium to undergo estrogen-driven repair, growth, and renewal after menstruation and parturition. Epithelial cells lining the uterine cavity undergo apoptosis during estrous cycles, and remnant cells can quickly restore this lining through a process known as re-epithelialization. It is presumed that adult stem/progenitor cells in the uterine stroma also contribute to re-epithelialization. However, the specific cell type(s) and the underlying mechanisms have not been determined. Herein, we use genetic lineage tracing assays in mice to identify Nestin+ perivascular cells as active contributors to re-epithelialization. Notch signaling maintains Nestin+ perivascular cells in a quiescent state, but these cells re-enter the cell cycle and differentiate into epithelial cells via estrogen-stimulated suppression of Notch signaling dependent on estrogen receptor alpha (ESR1). These findings demonstrate that perivascular cells support re-epithelialization and reveal a mechanism regulating the quiescence and activation of uterine perivascular cells.

Date: 2025
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DOI: 10.1038/s41467-025-65139-7

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