HUMAN DECIDUA AND FETAL MEMBRANES AS A PARACRINE SYSTEM

人蜕膜/胎膜系统作为可及性激素的潜力 将进一步探索自分泌/旁分泌模型，以阐明 松弛素类在胶原酶溶解和断裂局部控制中的作用 分娩时的胎膜。另一个挑战是我们的发现 第二个人类松弛蛋白基因(H1)在这个系统中表达。 这将通过研究放松的四个组成部分来实现 系统：基因表达、分泌控制、生物效应和 受体分布。 松弛蛋白H1和H2基因的表达和翻译产物，将 在子宫内膜/蜕膜、胎膜和胎盘中鉴定出 在整个周期和怀孕期间使用特定的核探针和抗体。 人参皂苷对蜕膜细胞松弛素分泌及mRNA水平的影响 一系列蜕膜和胎盘激素的松弛作用将在 在试管中。 人松弛素H2对胎膜/蜕膜的生物学作用 将寻求生产关键的胶原酶和抑制剂 在体外和体内。 宫内组织松弛素受体浓度的变化 将通过对周期和妊娠进行定量研究 放射自显影和与实验相关的结果 上面。 综合结果将提供对重大问题的洞察， 胎膜适应生长的局部控制 胎儿在妊娠的最后几周，以及正常自发的时间 胎膜破裂。这些研究将使我们更好地理解 胎膜早破，早产的主要原因 这会导致婴儿神经发育的发生率很高 减损。

The potential of the human decidua/fetal membrane system as an accessible autocrine/paracrine model will be further explored, in order to elucidate the role of relaxins in the local control of collagenolysis and the rupture of the fetal membranes at parturition. An added challenge is our finding that the second human relaxin gene (H1) is expressed in this system. This will be accomplished by studying the four components of the relaxin system: gene expression, control of secretion, biological effects and receptor distribution. Relaxin H1 and H2 gene expression and the translated products, will be identified in the endometrium/decidua, fetal membranes and placenta with specific riboprobes and antibodies throughout the cycle and pregnancy. The effect on decidual cell relaxin secretion and the mRNA levels for relaxins by a range of decidual and placental hormones will be studied in in vitro. The biological effects of human relaxin H2 on fetal membrane/decidual production of key collagenolytic enzymes and inhibitors will be sought both in vitro and in vivo. Changes in the concentration of relaxin receptors in intrauterine tissues will be studied through the cycle and gestation by quantitative autoradiography and the results related to those from the experiments above. The combined results will provide insights into significant problems, the local control of the accommodation of the fetal membranes to the growing fetus in the last weeks of pregnancy, and the timing of normal spontaneous membrane rupture. These studies will lead to a greater understanding of premature rupture of the fetal membranes, a major cause of premature birth which results in infants with a high incidence of neurodevelopmental impairment.