Torry Donald S, Mukherjea Debashree, Arroyo Juan, Torry Ronald J
Department of Medical Microbiology and Immunology and Obstetrics and Gynecology, Southern Illinois University School of Medicine, Springfield, Illinois 62794, USA.
J Soc Gynecol Investig. 2003 May;10(4):178-88. doi: 10.1016/s1071-5576(03)00048-0.
Essential requirements for successful gestation include the coordinated growth and differentiation of the placenta and the development of a functional placental vasculature. However, relatively little is known about factors that are responsible for regulating these functions. One angiogenic growth factor that might be involved in regulating both vascular endothelial cell and trophoblast function is placental growth factor (PGF).
Current published reports were surveyed and our own work was reviewed to highlight the expression, function, and potential significance of PGF at the human maternal-fetal interface.
PGF is highly expressed in trophoblasts during normal pregnancy, and its expression is significantly decreased in preeclampsia, an obstetric complication presumed to be associated with placental bed hypoxia and ischemia. In agreement with this, in vitro trophoblast expression of PGF can be down-regulated by low oxygen tension. The cognate receptor for PGF, fms-like tyrosine kinase receptor, is expressed on trophoblasts as well as vascular endothelial cells, suggesting that it has autocrine and paracrine functions. Accordingly, PGF can regulate proliferation in first trimester trophoblasts, apoptosis in term trophoblasts, and it can directly or indirectly regulate vascular growth, maturation, and permeability.
Many obstetric complications, most notably preeclampsia, are associated with aberrant trophoblast function and inadequate or dysfunctional vasculature within the developing placenta. The ability of PGF to influence trophoblast and vascular endothelial cells provides clear impetus for further studies to investigate the biological and clinical significance of PGF in normal and abnormal human pregnancies.
成功妊娠的基本要求包括胎盘的协调生长与分化以及功能性胎盘血管系统的发育。然而，对于调节这些功能的因素我们了解相对较少。一种可能参与调节血管内皮细胞和滋养层细胞功能的血管生成生长因子是胎盘生长因子（PGF）。
对当前已发表的报告进行了调研，并回顾了我们自己的研究工作，以突出PGF在人母胎界面的表达、功能及潜在意义。
在正常妊娠期间，PGF在滋养层细胞中高度表达，而在子痫前期其表达显著降低，子痫前期是一种推测与胎盘床缺氧和缺血相关的产科并发症。与此一致的是，低氧张力可下调体外培养的滋养层细胞中PGF的表达。PGF的同源受体，即fms样酪氨酸激酶受体，在滋养层细胞以及血管内皮细胞上均有表达，这表明它具有自分泌和旁分泌功能。因此，PGF可调节孕早期滋养层细胞的增殖、足月滋养层细胞的凋亡，并且它可以直接或间接调节血管的生长、成熟及通透性。
许多产科并发症，最显著的是子痫前期，与滋养层细胞功能异常以及发育中的胎盘内血管系统不足或功能失调有关。PGF影响滋养层细胞和血管内皮细胞的能力为进一步研究PGF在正常和异常人类妊娠中的生物学及临床意义提供了明确的动力。
