Expression of Ceramide Kinase （Cerk） and Related Regulation in Early Pregnant Uterus of Mice

Objective To investigate the expression of ceramide kinase (Cerk) and related regulation in mouse uterus during early pregnancy. Methods Several mouse models, including early pregnancy, pseudopregnancy, delayed or activated implantation, artificial decidualization, and steroid hormonal treatment were performed (n=10). Immunohistochemistry and in situ hybridization were used to detect the expression of Cerk protein and mRNA in uterus. Results Expression of Cerk mRNA and protein was strongly detected in the luminal and glandular epithelium on day 1 of pregnancy. However, Cerk mRNA and protein signals were strongly detected in the subluminal stroma surrounding the implanting blastocyst on day 5 and decidua from day 6 to day 8 whereas not in the luminal epithelium. The expression of Cerk in luminal and glandular epithelium of pseudopregnancy was similar to that of early pregnancy from day 1 to day 4 whereas on day 5 of pseudoprgenancy still with remarkable signals in the luminal epithelium. Under delayed implantation, no obvious Cerk expression was detected in the uterus. After delayed implantation was terminated by estrogen treatment and embryo implantation was initiated, both Cerk mRNA and protein were detected in the subluminal stroma surrounding the implanted blastocyst. A strong Cerk signal was detected in decidualized cells under artificial decidualization, whereas only a basal level of Cerk signal was observed in the control uterus which did not inject sesame oil. Progesterone induced a slight expression of Cerk in the luminal and glandular epithelium. Both estradiol and a combination of progesterone with estradiol strongly increased the level of Cerk signal in the luminal and glandular epithelium. Conclusion Cerk expression is under the regulation of progesterone and estrogen. The strong expression of Cerk in implantation site and decidua suggests that Cerk might play an important role during implantation and decidualization.     

A Preliminary Study of The Short Circuit Current （Isc） Responses of Endometria from Estrum and Bilateral Ovariectomy Female Rats

Objective To investigate the property of the endometrium ion transport in the normal estruation and ovariectomize rats. Methods The basic electrophysiological property of the endometrium was carried out by mean of the short circuit current （Isc） recording with the rats. Results The baseline Lsc and the transepithelial resistance （Rte） were different between the estruation and ovariectomized groups. Apical application of Na＋ channel blocker, amiloride （10 μmol/L）, or CFTR Cl- channel agonist, forskolin （10 μmol/L） did not significantly affect the Lc in the two groups. However, the 1sc in the model group was more sensitive to the CFTR Cl- channel blocker （glibenclamide, 1 mmol/L, apical） decreased about 27.0% （P〈0.05, n=6）, no remarkably changes in the estruation rats. While apical application CA CC CI-channel blocker, DIDS （4, 4 ＇-diisothiocyanostilbene- 2,2 ＇-disulfonic, 100 μmol/L）, the Isc was much more sensitive, percentage almost to 36.52% （P〈0.01） in the model group than that in the control Furthermore, basolateral application of bumetanide （100μmol/L）, a blocker of Na＋-K＋-2Cl- cotransport, didn＇t significantly reduce the Lc in the two groups. Conclusion The baseline Lsc and membrane resistance in the ovariectomize group is much higher than that in the normal estruation group, and the endometrial epithelium CI- secretion may be mediated by predominantly calcium-dependent CI- channels （CACC） and activating adenylate cyclase and apical cAMP-dependent Cl- channels （CFTR） in the model group with minor contributions in the control. Furthermore, the endometrial epithelium responses to different stimulants exists difference in the control and model group a likely mechanism for the ovary hormone.