Spatial and temporal patterns of expression of messenger RNA for insulin-like growth factors and their binding proteins in the placenta of man and laboratory animals

Spatial and temporal patterns of expression of messenger RNA for insulin-like growth factors and their binding proteins in the placenta of man and laboratory animals
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DOI:
10.1053/plac.1999.0498
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发表时间:
2000-05-01
期刊:
影响因子:
3.8
通讯作者:
Carter, AM
Carter, AM
中科院分区:
医学3区
文献类型:
--
作者:
Han, VKM;Carter, AM

文献摘要

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为了更好地了解胰岛素样生长因子(IGF-I和IGF-II)及其结合蛋白(IGFBPs 1-6)在胎盘发育和功能中的作用,重要的是要回顾物种之间在各自mRNA表达方面的相似性和差异。在人胎盘中,IGF-II mRNA表达于绒毛中胚层和早孕绒毛细胞滋养层,而不在合体滋养层。与此相反,在恒河猴胎盘,IGF-II mRNA表达在合体滋养层,但不是在绒毛膜中胚层。IGFBP-3 mRNA存在于这两个物种的胎盘绒毛的绒毛膜中胚层中,并可通过旁分泌机制调节IGF-II的作用。在啮齿动物胎盘中,IGF-II mRNA在胎儿中胚层和胎盘迷路的滋养层中表达。在豚鼠中,IGFBP-5 mRNA在边缘和小叶间合胞体中表达,IGF-PI mRNA在迷路中表达,IGF-II和IGFBP-5 mRNA之间的相互作用可能参与胎儿血管对胎盘的血管化。在绵羊胎盘中,IGF-II mRNA在滋养层中不表达,而在与滋养层相邻的中胚层表达,在人、猕猴和狒狒胎盘的基板中,绒毛外滋养层表达IGF-II mRNA,子宫蜕膜细胞表达IGFBP 1-6 mRNA。结论是在滋养层细胞侵入和蜕膜化过程中,IGF-Ⅱ和IGFBPs在灵长类胎盘的母胎界面上存在相互作用。蜕膜表达的IGFBP-1也可能与绒毛外滋养层表达的α 5 β 1整联蛋白相互作用。啮齿类动物的胎盘也属于侵入型。小鼠胎盘的糖原细胞与人绒毛外滋养层细胞相似,并表达IGF-II mRNA。然而,IGFBP mRNA在小鼠中的表达,如在豚鼠中,仅限于非蜕膜化的子宫内膜和子宫肌层。IGF-II mRNA在人和豚鼠胎盘滋养细胞侵入子宫血管时强烈表达。这些滋养层细胞表达的IGF-II和血管壁表达的IGFBPs之间可能发生相互作用。然而,这是可能的,IGFBPs表达的母体血管相关的过程是独立的滋养层入侵。因此,IGFBP-3 mRNA在非蜕膜羊胎盘的母体血管中高度表达。迄今为止的研究结果突出了IGF系统在人类和不同实验室动物胎盘中表达的多样性,甚至在密切相关的物种之间。将继续需要进行比较研究,以了解IGFs和IGFBPs在每个物种中的功能作用。(C)2000年哈考特出版社有限公司
To better understand the role of the insulin-like growth factors (IGF- I and -II) and their binding proteins (IGFBPs 1-6) in placental development and function, it is important to review similarities and differences between species in expression of the respective mRNAs. In human placenta, IGF-II mRNA is expressed in chorionic mesoderm and first trimester villous cytotrophoblast, but not in syncytiotrophoblast. In contrast, in rhesus monkey placenta, IGF-II mRNA is expressed in syncytiotrophoblast but not in chorionic mesoderm. IGFBP-3 mRNA is present in the chorionic mesoderm of placental villi from both these species and may modulate IGF-II action through a paracrine mechanism. In rodent placentae, IGF-II mRNA is expressed both in fetal mesoderm and in the trophoblast of the placental labyrinth. In guinea pig, where IGFBP-5 mRNA is expressed in the marginal and interlobular syncytium and IGF-PI mRNA in the labyrinth, interaction between IGF-II and IGFBP-5 mRNA may be involved in vascularization of the placenta by fetal vessels. In sheep placenta, IGF-II mRNA is expressed, not in the trophoblast layer, but in the fetal mesoderm immediately adjacent to it. In the basal plate of human, rhesus monkey and baboon placentae, extravillous trophoblasts express IGF-II mRNA and uterine decidual cells IGFBP 1-6 mRNAs. The inference is that there is interaction between IGF-II and IGFBPs at the maternal-fetal interface of the primate placenta during trophoblast invasion and decidualization. IGFBP-1 expressed by the decidua may also interact with alpha(5)beta(1) integrin expressed by the extravillous trophoblast. The placentae of rodents are also of the invasive type. Glycogen cells of the mouse placenta are analogous with human extravillous trophoblast and express IGF-II mRNA. However, expression of IGFBP mRNAs in the mouse, as in the guinea pig, is confined to non-decidualized endometrium and myometrium. IGF-II mRNA is strongly expressed by trophoblasts invading uterine vessels in human and guinea pig placentae. Interactions probably occur between IGF-II expressed by these trophoblasts and IGFBPs expressed in the vessel walls. However, it is possible that IGFBPs expressed by maternal vessels are associated with processes that are independent of trophoblast invasion. Thus, IGFBP-3 mRNA is highly expressed in the maternal blood vessels of the non-deciduate sheep placenta. Findings to date highlight the diversity in the expression of the IGF system among placentae of man and different laboratory animals, and even between closely related species. Comparative studies will continue to be required to understand the functional role of IGFs and IGFBPs in each species. (C) 2000 Harcourt Publishers Ltd.