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Mapping Uterine Remodeling from Pregnancy to a New Homeostatic State

Pregnancy drives uterine remodeling through rapid anatomical expansion and scar-free postpartum repair, yet how the organ reconstructs its cellular architecture after birth remains incompletely understood. Here, we present single-cell transcriptomic profiling of 698,631 cells derived from the whole mouse uterus across five distinct stages centered around parturition: Non-pregnant Control, late…

Pregnancy causes significant changes in the uterus through rapid expansion and subsequent repair without scarring. However, the precise way the organ remodels its cellular structure after giving birth is still not fully understood. To investigate this, researchers analyzed the transcriptome of 698,631 cells from the mouse uterus at five key stages surrounding birth: a control non-pregnant state, late gestation at embryonic day 16.5, and postpartum days 1, 7, and 30.

This analysis identified 16 different cell lineages within the uterus, including epithelial, stromal, endothelial, and immune cells. While the uterus shrinks back to its original size relatively quickly, the cellular makeup, gene expression patterns, and intercellular communication networks do not return to their pre-pregnancy state.

Instead, the tissue undergoes a series of five overlapping transcriptional programs after birth, with individual cells both shedding their pregnancy-associated traits and developing repair-related characteristics. One month postpartum, the uterus has established a new, stable state that differs from its pre-pregnancy condition, indicating a shift toward a novel homeostatic configuration rather than reverting to a completely normal state.

This research sheds light on the specific stages of cellular recovery following physiological stress and how some aspects of the uterus adapt to new baseline conditions.

Written by urgent.news from bioRxiv's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.

Read the original at biorxiv.org →

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