Han V K, Carter A M, Chandarana S, Tanswell B, Thompson K
Department of Paediatrics, Lawson Research Institute, University of Western Ontario, London, Canada.
Placenta. 1999 May;20(4):361-77. doi: 10.1053/plac.1998.0389.
To determine the temporal and spatial distribution of insulin-like growth factor (IGF) and its family of binding proteins (IGFBPs), guinea-pig yolk sac and chorioallantoic placentae were collected at 15, 20, 25, 29, 44-45, 55 and 65-66 days of gestation. Messenger RNAs for IGF I, IGF II and IGFBP 1-6 were identified in tissue sections by in situ hybridization, using 35S-cRNA probes. Epithelial and mesenchymal cell types were identified by immunohistochemistry for cytokeratin and vimentin, respectively. At 15 days of gestation, IGF-II mRNA was expressed in ectoplacental mesoderm, cytotrophoblasts and syncytiotrophoblast, and IGFBP-5 mRNA was detected in the syncytiotrophoblast. In the mid-gestation placenta, IGFBP-5 mRNA was expressed in the marginal and interlobular syncytium and IGF-II mRNA in the labyrinth. Near term, when expansion of the labyrinth was complete, IGFBP-5 mRNA was coexpressed with IGF-II mRNA in the marginal and interlobular syncytium. These observations suggest that interaction between IGF-II and IGFBP-5 plays a role in the vascularization of the placenta by fetal vessels. IGF-II mRNA was not expressed in the maternal tissues at any gestational age. IGFBP-2, -3 and -5 mRNAs were expressed in the endometrial stroma at 7-12 days of gestation but, following establishment of the placenta, IGFBP mRNAs were more abundant in the myometrium than in the decidua. IGF-II mRNA was detected in trophoblasts invading the walls of maternal vessels, and the endothelium of the preplacental vessels expressed IGFBP-4 mRNA, while IGFBP-2 and IGFBP-5 mRNAs were present in the tunica media of mesometrial arteries that had not been invaded by trophoblast. These findings suggest that IGF-II produced by the trophoblast acts in an autocrine and/or paracrine fashion to promote trophoblast invasion and that this process is modulated by interaction with IGFBPs present in maternal tissues.
为了确定胰岛素样生长因子（IGF）及其结合蛋白家族（IGFBPs）的时空分布，在妊娠15、20、25、29、44 - 45、55和65 - 66天时收集豚鼠卵黄囊和绒毛膜尿囊胎盘。使用35S - cRNA探针，通过原位杂交在组织切片中鉴定IGF I、IGF II和IGFBP 1 - 6的信使核糖核酸。分别通过细胞角蛋白和波形蛋白的免疫组织化学鉴定上皮细胞和间充质细胞类型。在妊娠15天时，IGF - II信使核糖核酸在外胎盘间充质、细胞滋养层和合体滋养层中表达，IGFBP - 5信使核糖核酸在合体滋养层中检测到。在妊娠中期胎盘，IGFBP - 5信使核糖核酸在边缘和小叶间合体中表达，IGF - II信使核糖核酸在迷路中表达。接近足月时，当迷路扩张完成，IGFBP - 5信使核糖核酸与IGF - II信使核糖核酸在边缘和小叶间合体中共表达。这些观察结果表明，IGF - II与IGFBP - 5之间的相互作用在胎儿血管对胎盘的血管化过程中起作用。在任何妊娠年龄，IGF - II信使核糖核酸均未在母体组织中表达。IGFBP - 2、- 3和- 5信使核糖核酸在妊娠7 - 12天时在内膜基质中表达，但在胎盘形成后，IGFBP信使核糖核酸在子宫肌层中比在蜕膜中更丰富。在侵入母体血管壁的滋养层细胞中检测到IGF - II信使核糖核酸，胎盘前血管的内皮表达IGFBP - 4信使核糖核酸，而IGFBP - 2和IGFBP - 5信使核糖核酸存在于未被滋养层侵入的子宫系膜动脉的中膜中。这些发现表明，滋养层产生的IGF - II以自分泌和/或旁分泌方式发挥作用，促进滋养层侵袭，并且这一过程通过与母体组织中存在的IGFBPs相互作用而受到调节。
