POSTIMPLANTATION MODIFICATION OF SPIRAL ARTERIES

我们的项目研究了胎儿滋养层细胞 侵入并改变供应动脉的螺旋动脉壁， 胎盘充分的侵入和重塑提供了正常的血液 胎盘供应。 侵入不足与 妊娠高血压、先兆子痫、宫内发育迟缓 和其它问题。 我们使用猕猴模型，因为它是为数不多的 这是一种与人类动脉侵犯相似的物种。 这些研究还利用相同的材料来分析胎盘生长 和一般的差异。 在过去的一年里，我们 在若干领域取得重大进展。 在1994年，我们完成了一盏灯， 厚基底发育的电镜研究 猕猴胎盘的锚定绒毛中的膜状结构。 这种结构似乎是重要的分离胎儿结缔组织 来自母体来源的细胞的组织成分。 我们还完成了， 发表了一项研究，证明存在72 KD的IV型 胶原酶在侵袭性滋养层细胞迁移到 螺旋动脉的壁 我们还完成并发表了一项研究， 猕猴胎盘绒毛板的生长和发育 并将其与胎盘生长联系起来。 最后，我们完成了， 发表了一项免疫细胞化学研究， 猕猴胎盘的不同隔室，使用两种核抗体 蛋白KI-67和puna。 这使我们能够证明， 动脉滋养层细胞是非增殖性的，因此必须全部 从其他地方迁移到这个网站。 初步研究已经开始， 各种粘附分子在动脉中的表达，包括 整联蛋白、n-cam和其他蛋白以及各种 动脉壁的细胞外基质分子

Our project investigates the mechanisms by which fetal trophoblast cells invade and modify the walls of the spiral arteries supplying the placenta. Adequate invasion and remodeling provide for a normal blood supply at the placenta. Inadequate invasion has been associated with hypertensive pregnancies, pre-eclampsia, intrauterine growth retardation and other problems. We use the macaque model since it is one of the few species available that has artery invasion similar to that in the human. The studies also utilize the same material to analyze placental growth and differentiation in general. During the past year we have made significant progress in a number of areas. In 1994 we completed a light and electron microscopic study of the development of a thick basement membrane-like structure in the anchoring villi of the macaque placenta. This structure appears to be important in isolating fetal connective tissue elements from maternally-derived cells. We also completed and published a study demonstrating the presence of a 72 KD type IV collagenase at sites where the invasive trophoblast cells migrate into the wall of the spiral arteries. We also completed and published a study of growth and development of the chorionic plate of the macaque placenta and related it to placental growth in general. Finally, we completed and published an immunocytochemical study examining cell proliferation in various compartments of macaque placentas using antibodies to two nuclear proteins KI-67 and puna. This enabled us to demonstrate that the arterial trophoblast cells were non-proliferative and therefore must all migrate to this site from elsewhere. Preliminary studies have begun on expression of various adhesion molecules in the arteries, including integrins, n-cam and others as well as the appearance of various extracellular matrix molecules in the arterial wall.