| Embryo implantation is a complex sequential process, playing a pivotal role in successfulpregnancy. Endometrial receptivity is closely related to the process of embryo implantation. Recently, studies foucused on the transformation of pinopodes and the changes of cytokines as well as adhesion moleculars in endometrium, while little is known about the relationship between the changes of cytokines, adhesion moleculars and the whole steroid level, therefore the mechanism remains poorly understood. NF κ. B is a general transcript factor, mediating one of the classics signal pathways through membrane receptors. Many animals, including rodent and primate, bear expression of NF K B in their endometrium, and the expression of endometrial NF K B in mouse and human related to their estrogen and progestin. LIF is a critical cytokines in embryo implantation. We traced down the expression, function and regulation of LIF in mouse endometrium in last couples years, and found that LIF can stimulate the expression of integrin β 3 , which is regarded as the molecular marker of endometrial receptivity. Estrogen and progestin can regulate the expression of LIF, It maybe hypothesized that there is mutual modulation between LIF and NF K B, while we reached little to that. Objectives:Through different treatment with in vitro mouse endometrial stromal cell and ovariectomized mouse, to investigate the expression of NF K B and it't nuclear translocation, and explore the possible mechanism of estrogen, progesterone and LIF involving in NF K B signaling and the possible establishment of receptivity. Methods and Materials:Female KM mouse aged 8-12 weeks and weightted 25-30g were taken in the present study, Purified endometrial stromal cells of mouse were employed for in vitro experiments, cells were divided randomly into groups according to given treatments, priscribed with 17-β-estradiol, progesterone, 17-β-estradiol combined progesterone, LIF, 17- β -estradiol combined progesterone and together with Anti-LIF, respectively. The expressions of NF K B were determined by immunocytochmestry or Fluorescence immunocytochmestry. Ovariectomized mouse models were used in in vivo experiment, Sham-operation group as positive control, received s.c. injection ofdifferent dose of either estrogen or progesterone or estrogen combined with progesterone. Investigate the endometrium mRNA level of NF K B and I K B through real-time PCR, and immunohistochemistry for protein. Results:In vitro mouse endometrial cell all could express NF K B. The cells with positive cytoplasma NF K B haven't statistically deviation compared with the negative control group in sereies estrogen treated time (p>0. 05) . The population of cells with nuclear positive NF K B peaked in Ihr, significantly higher than the control and other time point (p<0. 01), indicated that estrogen could regulate the expression of NF K B and it's nuclear translocation. During the period of Ihr to 2hr after the treatment of progesterone, the nuclear NFKB increased remarkably than the control and other time point group. Priscribed estradiol combined progesterone, the expression of NF K B both in cytoplasm and nucleus is higher than the control group (p<0.05) in 1, 2, 4 and 8 hr(s) points, furthermore, the nuclear NF K B elevated distinctly with the control group in 1 and 2 hr(s) points (p<0. 001).Given different dose of LIF(Ing/ml, lOng/ml, lOOng/ml), the expression of NFicB increased as dose-dependent manner. LIF(10ng/ml) could imcrease NFicB level both in the cytoplasma and nuclear, suggested that appropriate dose of LIF could not only up-regulate the NFicB, but also promote its nucleus translocation.Ihr or 2hrs after treatments of estradiol combined with progesterone, the addition of Anti-LIF obviously suppressed the NFicB expression(p<0.05). When estradiol combined with progesterone and Anti-LIF at the same time, Anti-LIF of lug/ml group got significant deviation compared with 5ug/ml and lOug/ml groups, while the latter two are similar to each other(p>0.05).in vivo experiments, proges...
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