Placental development in normal and compromised pregnancies - A review
Placental development in normal and compromised pregnancies - A review
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DOI：
10.1053/plac.2002.0792
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发表时间：
2002-04-01
期刊：
影响因子：
3.8
通讯作者：
Anthony, RV
中科院分区：
文献类型：
--
作者：
Regnault, TRH;Galan, HL;Anthony, RV
胎儿宫内生长受限(IUGR)是导致婴儿死亡和发病的重要原因。现在很明显，IUGR婴儿成年后患冠心病、2型糖尿病、高血压和中风的几率更高。因此，胎儿发育不仅影响围产期的结局，也影响成人的幸福感。IUGR的病因很多，但往往与胎盘结构和功能异常有关。着床和胎盘形成过程需要产生过多的生长因子、细胞黏附分子、细胞外基质蛋白、激素和转录因子。其中许多在IUGR妊娠的胎盘中表现出变化的表达。然而，很难完全评估它们在人类胎盘功能不全(PI)发展过程中的作用，强调了建立动物模型的必要性。利用绵羊PI-IUGR模型，观察了血管内皮生长因子、胎盘生长因子及其共同受体、血管生成素-2及其受体Tie-2的表达变化，发现这些生长因子的变化与胎盘血管结构和功能的急慢性变化有关。这些研究和其他研究为胎盘功能不全的发育年表提供了必要的洞察力。(C)2002年IFPA和爱思唯尔科学有限公司。
Intrauterine growth restriction (IUGR) is a significant cause of infant mortality and morbidity. It is now clear that IUGR infants exhibit higher rates of coronary heart disease, type 2-diabetes, hypertension and stroke as adults. Therefore, fetal growth not only impacts the outcome of the perinatal period, but also impacts adult well-being. The etiologies of IUGR are numerous, but are often associated with abnormalities in placental structure and function. The process of implantation and placentation requires the production of a plethora of growth factors, cell-adhesion molecules, extracellular matrix proteins, hormones and transcription factors. Many of these exhibit altered expression within the placenta of IUGR pregnancies. However, it has been difficult to fully assess their role during the development of placental insufficiency (PI) in the human, underscoring the need for animal models. Using an ovine model of PI-IUGR we have observed changes in the expression of vascular endothelial growth factor, placental growth factor, their common receptors, as well as angioproietin 2 and its receptor, Tie 2. We found that changes in these growth factors can be associated with both acute and chronic changes in placental vascular structure and function. These studies and others are providing needed insight into the developmental chronology of placental insufficiency. (C) 2002 IFPA and Elsevier Science Ltd.