DEK对人子宫内膜蜕膜化的调节作用

The Regulation of DEK in Human Endometrial Decidualization

为探讨DNA结合蛋白果蝇Eph激酶(Drosophila Eph kinase,DEK)对人子宫内膜基质蜕膜化的调节作用和途径,该研究采用qPCR(Real-time quantitative polymerase chain reaction)、免疫组化(immunohistochemical)和蛋白印迹(Western blot)分别检测人子宫内膜增生期、分泌期和蜕膜组织中DEK基因和蛋白的表达;利用siRNA抑制基质细胞和蜕膜细胞的DEK,再用细胞流式技术、细胞免疫荧光、qPCR、细胞碱性磷酸酶脂显色和Western blot检测DEK沉默后细胞的变化。结果显示,蜕膜组织中DEK mRNA表达水平低于增生期和分泌期(P<0.05),蜕膜组织中DEK蛋白表达水平高于增生期和分泌期(P<0.05);抑制基质细胞DEK会使细胞增殖和分化能力降低,从而抑制基质细胞蜕膜化;抑制蜕膜细胞DEK可使细胞凋亡增加,DNA损伤情况加剧,导致蜕膜细胞的维持和发展受到影响。综上,该研究初步证实,DEK可能通过调控细胞蜕膜化而参与胚胎着床过程,其可能途径与其通过调控细胞增殖、分化、凋亡和核损伤有关。

In this study, to investigate the regulation of endometrial decidualization by Drosophila Eph kinase （DEK） a DNA-binding protein, the expression pattern of DEK in human tissue （proliferative, secretory and decidualization） was detected by Real-time quantitative polymerase chain reaction （qPCR）, immunohistochemistry （IHC） and Western blot. Human uterine stromal and decidual cells were inhibited the expression of DEK. Then the proliferation, differentiation, apoptosis and DNA damage of cells were detected. Our results revealed that the expression pattern ofDEK mRNA in decidualization was significantly lower than that in proliferative and secretory groups. The expression pattern of DEK protein in decidualization was significantly higher than that in proliferative and secretory groups. DEK inhibited in stromal cells causes decrease in proliferation and differentiation ability. DEK inhibited in decidual cells causes increases apoptosis and DNA damage. Taken together, in the present study, we primarily indicated that DEK possibly through regulation of cell decidualization to participate in embryo implantation process. DEK through the regulation of cell proliferation, differentiation, apoptosis and DNA damage is involved in the regulation of decidualization.