Unidad de Reproducción y Desarrollo, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile.
Reproduction. 2010 Mar;139(3):631-44. doi: 10.1530/REP-09-0218. Epub 2009 Dec 23.
Estradiol (E(2)) accelerates oviductal egg transport through intraoviductal non-genomic pathways in unmated rats and through genomic pathways in mated rats. This shift in pathways has been designated as intracellular path shifting (IPS), and represents a novel and hitherto unrecognized effect of mating on the female reproductive tract. We had reported previously that IPS involves shutting down the E(2) non-genomic pathway up- and downstream of 2-methoxyestradiol. Here, we evaluated whether IPS involves changes in the genomic pathway too. Using microarray analysis, we found that a common group of genes changed its expression in response to E(2) in unmated and mated rats, indicating that an E(2) genomic signaling pathway is present before and after mating; however, a group of genes decreased its expression only in mated rats and another group of genes increased its expression only in unmated rats. We evaluated the possibility that this difference is a consequence of an E(2) non-genomic signaling pathway present in unmated rats, but not in mated rats. Mating shuts down this E(2) non-genomic signaling pathway up- and downstream of cAMP production. The Star level is increased by E(2) in unmated rats, but not in mated rats. This is blocked by the antagonist of estrogen receptor ICI 182 780, the adenylyl cyclase inhibitor SQ 22536, and the catechol-O-methyltransferase inhibitor, OR 486. These results indicate that the E(2)-induced gene expression profile in the rat oviduct differs before and after mating, and this difference is probably mediated by an E(2) non-genomic signaling pathway operating on gene expression only in unmated rats.
雌二醇（E2）通过未交配大鼠输卵管内的非基因组途径和交配大鼠的基因组途径加速输卵管卵运输。这种途径的转变被指定为细胞内途径转变（IPS），代表了交配对雌性生殖道的一种新的、迄今为止尚未被认识的影响。我们之前曾报道过，IPS 涉及关闭 2-甲氧基雌二醇上下游的 E2 非基因组途径。在这里，我们评估了 IPS 是否也涉及基因组途径的变化。使用微阵列分析，我们发现一组共同的基因在未交配和交配大鼠中对 E2 的反应改变了其表达，表明在交配前后存在 E2 基因组信号通路；然而，一组基因仅在交配大鼠中表达降低，另一组基因仅在未交配大鼠中表达增加。我们评估了这种差异是否是未交配大鼠中存在而交配大鼠中不存在的 E2 非基因组信号通路的结果。交配会关闭 cAMP 产生上下的 E2 非基因组信号通路。E2 在未交配大鼠中增加 Star 水平，但在交配大鼠中不增加。这被雌激素受体拮抗剂 ICI 182 780、腺苷酸环化酶抑制剂 SQ 22536 和儿茶酚-O-甲基转移酶抑制剂 OR 486 阻断。这些结果表明，大鼠输卵管中 E2 诱导的基因表达谱在交配前后不同，这种差异可能是由仅在未交配大鼠中作用于基因表达的 E2 非基因组信号通路介导的。
