Function of Growth Arrest Specific 1 on Endometrial Decidualization in Early Pregnant Mice
TAN Qiman, XU Hanting, LI Nanyan, LIU Xueqing, HE Junlin, DING Yubin, WANG Yingxiong, GAO Rufei, CHEN Xuemei*
The purpose of this study was to explore the expression of Gas1 (growth arrest specific 1) in the endometrium of early pregnant mice and its role in decidualization. The expression of Gas1 in the endometrium of normal and pseudopregnant mice was detected by immunohistochemistry, Western blot and RT-qPCR. In vivo and in vitro models of artificial induced decidualization were constructed respectively, and the expression of Gas1 in the models was detected by Western blot and RT-qPCR. Gas1 was overexpressed in primary endometrial stromal cells, and its effects on decidualization, proliferation and apoptosis were detected by Western blot, RT-qPCR and flow cytometry. The results showed that Gas1 expression at implantation sites was significantly lower than that at the interimplantation sites of pregnant mice from D5 to D7. Artificial-induced decidualiazation inhibited the expression of Gas1 both in vivo and in vitro. Overexpression of Gas1 disturbed the proliferation and apoptosis of stromal cells and impaired decidualization. In addition, the expression of Gas1 in endometrial tissues of spontaneous abortion patients was significantly higher than that in the normal early pregnancy group. This study tentatively demonstrated that Gas1 might affect the decidualization of mouse endometrial stromal cells by mediating cell proliferation and apoptosis, thereby playing an important role in embryo implantation.
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