title: Placental development in normal and compromised pregnancies-- a review.
abstract: 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.
authors.affiliation: Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
authors.forename: T R H
authors.initials: TR
authors.lastname: Regnault
authors.forename: H L
authors.initials: HL
authors.lastname: Galan
authors.forename: T A
authors.initials: TA
authors.lastname: Parker
authors.forename: R V
authors.initials: RV
authors.lastname: Anthony
mesh_terms: D000328:Adult; D043925:Angiogenesis Inducing Agents / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D008833:Microcirculation / Q000648:ultrastructure; D009024:Morphogenesis; D018919:Neovascularization, Physiologic / Q000502:physiology; D010920:Placenta / Q000098:blood supply / Q000196:embryology; D010927:Placental Insufficiency / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D010929:Placentation; D011247:Pregnancy; D017978:Receptors, Growth Factor / Q000378:metabolism; D012756:Sheep; D014327:Trophoblasts / Q000378:metabolism / Q000648:ultrastructure
chemical_list: D043925:Angiogenesis Inducing Agents; D017978:Receptors, Growth Factor