Lewis X(Le x) is stage specifically expressed on the surface of mammalian embryos. Histochemical evidences have showed that Le x is expressed in endometrium, and may be controlled by ovarian hormones. It has been repo...Lewis X(Le x) is stage specifically expressed on the surface of mammalian embryos. Histochemical evidences have showed that Le x is expressed in endometrium, and may be controlled by ovarian hormones. It has been reported that FUT9 gene is the real specific gene encoding α1, 3 fucosyltransferase for the synthesis of terminal fucose of Le x. In this article, the transcription of FUT9 and expression of Le x oligosaccharide antigen in mouse endometrium were investigated. The mice(22～25 g) were selected and treated as follows:(1) Estrous: females were checked by vaginal smears to determine their stage of estrus;(2) Early pregnancy: females were mated with males(1∶1), and the day of vaginal plug appearance was considered as day 1 of pregnancy;(3) Hormone replacement: after ovariectomy, mice were given subcutaneously estradiol benzoate and progesterone daily for 4 days. The results showed that the transcription level of FUT9 gene was:(1) periodically changed during estrous cycle: highest at estrus stage, and lowest at metestrus stage;(2) decreased obviously during early pregnancy, then maintained at a lower level from day 3 to day 5;(3) increased in the estradiol treatment group, and decreased obviously in the progesterone treatment group, and was at a middle level in the group treated with both estradiol and progesterone;(4) level of Le x carrying proteins on the surface of endometrium did it coincide fully with that of FUT9 gene transcription, which indicated that other factors may be also involved in the regulation of Le x expression in addition to the hormones. In summary, the expression of FUT9 gene in mouse endometrium is regulated by ovarian hormones, being up regulated by estrogen and down regulated by progesterone.展开更多
文摘Lewis X(Le x) is stage specifically expressed on the surface of mammalian embryos. Histochemical evidences have showed that Le x is expressed in endometrium, and may be controlled by ovarian hormones. It has been reported that FUT9 gene is the real specific gene encoding α1, 3 fucosyltransferase for the synthesis of terminal fucose of Le x. In this article, the transcription of FUT9 and expression of Le x oligosaccharide antigen in mouse endometrium were investigated. The mice(22～25 g) were selected and treated as follows:(1) Estrous: females were checked by vaginal smears to determine their stage of estrus;(2) Early pregnancy: females were mated with males(1∶1), and the day of vaginal plug appearance was considered as day 1 of pregnancy;(3) Hormone replacement: after ovariectomy, mice were given subcutaneously estradiol benzoate and progesterone daily for 4 days. The results showed that the transcription level of FUT9 gene was:(1) periodically changed during estrous cycle: highest at estrus stage, and lowest at metestrus stage;(2) decreased obviously during early pregnancy, then maintained at a lower level from day 3 to day 5;(3) increased in the estradiol treatment group, and decreased obviously in the progesterone treatment group, and was at a middle level in the group treated with both estradiol and progesterone;(4) level of Le x carrying proteins on the surface of endometrium did it coincide fully with that of FUT9 gene transcription, which indicated that other factors may be also involved in the regulation of Le x expression in addition to the hormones. In summary, the expression of FUT9 gene in mouse endometrium is regulated by ovarian hormones, being up regulated by estrogen and down regulated by progesterone.
文摘目的探讨岩藻糖基转移酶2(fucosyltransferase 2,FUT2)在A385T位点和G428A位点的基因多态性与炎症性肠病(inflammatory bowel disease,IBD)易感性的关系.方法计算机检索EMBASE、PubMed、EBM Reviews、Ovid、Springer、中国期刊全文数据库(CNKI)、万方数字化期刊全文数据库,查找关于FUT2基因多态性与IBD相关性的研究,对纳入文献进行质量评价,提取有效数据,使用Review Manager 5.3和Stata 12.0软件进行Meta分析,并用Begg's漏斗图进行发表偏倚检测.结果共纳入10篇文献,病例组3682例,对照组5470例.各种遗传模型在溃疡性结肠炎(ulcerative colitis,UC)中,显性遗传模型[(AA+AT)vs TT]中OR=1.00(95%CI:0.83-1.21),[(GG+GA)vs AA]中OR=1.05(95%CI:0.81-1.36);隐性遗传模型[(AT+TT)vs AA]中OR=0.96(95%CI:0.73-1.25),[(GA+AA)vs GG]中OR=0.70(95%CI:0.36-1.36);共显性遗传模型中(AA vs TT)中OR=1.02(95%CI:0.82-1.27),(GG vs AA)中OR=1.23(95%CI:0.93-1.63);等位基因模型(A vs T)中OR=1.06(95%CI:0.95-1.17),(G vs A)中OR=1.18(95%CI:0.68-2.04).各种遗传模型在克罗恩病(Crohn's disease,CD)中,显性遗传模型[(AA+AT)vs TT]中OR=0.60(95%CI:0.43-0.85),[(GG+GA)vs AA]中OR=0.51(95%CI:0.38-0.70);隐性遗传模型[(AT+TT)vs AA]中OR=0.99(95%CI:0.73-1.35),[(GA+AA)vs GG]中OR=1.49(95%CI:1.17-1.91);共显性模型(AA vs TT)中OR=1.37(95%CI:0.95-1.98),(GG vs AA)中OR=0.46(95%CI:0.33-0.65);等位基因模型(G vs A)中OR=0.67(95%CI:0.57-0.79),(G vs A)中OR=0.67(95%CI:0.57-0.79).结论 FUT2 A385T与G428A基因多态性与UC易感性无关.亚洲人群中FUT2 A385T上基因型TT会增加CD的发病风险.FUT2 G428A多态性与CD相关,携带等位基因A会增加CD的易感性.
