Previously, using the Keratin5-Cre transgenic mouse model we reported that female Lgr4- conditional KO mice (Lgr4K5 KO) showed subfertility with defective stromal decidualization due to abnormal development of the uterine gland. However, the impact of the LGR4 defect on luminal epithelial cells was not investigated in the previous report. Here, we focused on the receptive state of the luminal epithelium in Lgr4K5 KO mice that received ovarian hormone treatment. In Lgr4K5 KO mice, progesterone failed to inhibit the luminal epithelial cell proliferation. Immunohistochemical and qRT-PCR analyses revealed downregulated progesterone signaling in the uterus of Lgr4K5 KO mice. These results demonstrated that LGR4 is essential for the acquisition of endometrial receptivity through ovarian hormone signaling.
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