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The endometrial mesenchymal stromal\/stem cells (eMSC) contribute to this process. Notch signaling is essential for homeostasis of somatic stem cells. However, its role in eMSC remains unclear. We show with gain- and loss-of-function experiments that activation of Notch signaling promotes eMSC maintenance, while inhibition induces opposite effect. The activation of Notch signaling better maintains eMSC in a quiescent state. However, these quiescent eMSC can re-enter the cell cycle depending on the Notch and Wnt activities in the microenvironment, suggesting a crosstalk between the two signaling pathways. We further show that the Notch signaling is involved in endometrial remodeling event in a mouse menstrual-like model. Suppression of Notch signaling reduces the proliferation of Notch1<jats:sup>+<\/jats:sup> label-retaining stromal cells and delays endometrial repair. 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