Regnault T R H, Galan H L, Parker T A, Anthony R V
Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
Placenta. 2002 Apr;23 Suppl A:S119-29. doi: 10.1053/plac.2002.0792.
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 angiopoietin 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.
宫内生长受限（IUGR）是婴儿死亡和发病的一个重要原因。现在很清楚，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，胎儿生长不仅影响围产期结局，还影响成人健康。IUGR的病因众多，但通常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大量生长因子、细胞粘附分子、细胞外基质蛋白、激素和转录因子。其中许多在IUGR妊娠的胎盘内表达发生改变。然而，很难全面评估它们在人类胎盘功能不全（PI）发展过程中的作用，这凸显了对动物模型的需求。使用PI-IUGR绵羊模型，我们观察到血管内皮生长因子、胎盘生长因子、它们的共同受体以及血管生成素2及其受体Tie 2的表达变化。我们发现这些生长因子的变化可能与胎盘血管结构和功能的急性和慢性变化有关。这些研究以及其他研究正在为胎盘功能不全的发育时间顺序提供必要的见解。
