The involvement of the progesterone receptor in PIBF and Gal-1 expression in the mouse endometrium (CROSBI ID 275357)
Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija
Podaci o odgovornosti
Mulac‐Jeričević, Biserka ; Šućurović, Sandra ; Gulic, Tamara ; Szekeres‐Bartho, Julia
engleski
The involvement of the progesterone receptor in PIBF and Gal-1 expression in the mouse endometrium
Problem The progesterone-regulated genes, PIBF and Gal-1, are key players in the feto-maternal immunological interaction. This study aims to investigate the expression of PIBF and Gal-1 in WT and progesterone receptor KO models as well as subsequent effects of PIBF on decidualization of stromal cells. Method of the study PRAKO, PRBKO and PRKO BALB/c mice were used for assessing the role of PR isoforms in PIBF induction. PIBF- and Gal-1 mRNA expression in the uterus was tested by real-time PCR. The effect of PIBF on decidualization of endometrial stromal cells was verified by anti- desmin immunofluorescence. Immunohistochemistry was used for testing PIBF expression in the uterus. Gal-1, ER alpha and PR positive decidual NK cells were detected by immunofluorescence. Results PIBF mRNA was significantly increased in progesterone-treated WT mice, but not in PRKO and PRAKO mice. PIBF protein expression was reduced in the endometria of PRKO and PRAKO, but not in PRBKO mice. During a 6-day culture, PIBF induced decidual transformation of endometrial stromal cells. PIBF expression in the mouse uterus was highest during the implantation window, while Gal-1 mRNA expression continuously increased between day 2.5 and day 11.5 of gestation. Decidual NK cells express Gal-1 and ER alpha, but not PR at day 7.5 murine pregnancy. Conclusion PIBF produced via engagement of PRA, is highly expressed in the endometrium during the implantation window, and plays a role in decidualization. The concerted action of PIBF and Gal-1 might contribute to the low cytotoxic activity of decidual NK cells.
decidual NK cells ; decidualization ; Gal-1 ; PIBF ; progesterone receptor isoforms
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Podaci o izdanju
81 (5)
2019.
e13104
9
objavljeno
1046-7408
10.1111/aji.13104
Povezanost rada
Temeljne medicinske znanosti