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Publication : Expression of PIK3IP1 in the murine uterus during early pregnancy.

First Author  Teasley HE Year  2018
Journal  Biochem Biophys Res Commun Volume  495
Issue  4 Pages  2553-2558
PubMed ID  29289536 Mgi Jnum  J:270158
Mgi Id  MGI:6277250 Doi  10.1016/j.bbrc.2017.12.154
Citation  Teasley HE, et al. (2018) Expression of PIK3IP1 in the murine uterus during early pregnancy. Biochem Biophys Res Commun 495(4):2553-2558
abstractText  The ovarian steroid hormones, estrogen (E2) and progesterone (P4), are essential regulators of uterine functions necessary for development, embryo implantation, and normal pregnancy. ARID1A plays an important role in steroid hormone signaling in endometrial function and pregnancy. In previous studies, using high density DNA microarray analysis, we identified phosphatidylinositol-3-kinase interacting protein 1 (Pik3ip1) as one of the genes up-regulated by ARID1A. In the present study, we performed real-time qPCR and immunohistochemistry analysis to investigate the regulation of PIK3IP1 by ARID1A and determine expression patterns of PIK3IP1 in the uterus during early pregnancy. The expression of PIK3IP1 was strong at the uterine epithelial and stromal cells of the control mice. However, expression of PIK3IP1 was remarkably reduced in the Pgr(cre/+)Arid1a(f/f) mice and progesterone receptor knock-out (PRKO) mice. During early pregnancy, PIK3IP1 expression was strong at day 2.5 of gestation (GD 2.5) and then slightly decreased at GD 3.5at the epithelium and stroma. After implantation, PIK3IP1 expression was detected at the secondary decidualization zone. To determine the ovarian steroid hormone regulation of PIK3IP1, we examined the expression of PIK3IP1 in ovariectomized control, Pgr(cre/+)Arid1a(f/f), and PRKO mice treated with P4 or E2. P4 treatment increased the PIK3IP1 expression at the luminal and glandular epithelium of control mice. However, the PIK3IP1 induction was decreased in both the Pgr(cre/+)Arid1a(f/f) and PRKO mice, compared to controls. Our results identified PIK3IP1 as a novel target of ARID1A and PGR in the murine uterus.
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