title: Placental Ischemia and Resultant Phenotype in Animal Models of Preeclampsia.
abstract: Preeclampsia is new onset (or worsening of preexisting) hypertension that occurs during pregnancy. It is accompanied by chronic inflammation, intrauterine growth restriction, elevated anti-angiogenic factors, and can occur with or without proteinuria. Although the exact etiology is unknown, it is thought that preeclampsia begins early in gestation with reduced uterine spiral artery remodeling leading to decreased vasculogenesis of the placenta as the pregnancy progresses. Soluble factors, stimulated by the ischemic placenta, shower the maternal vascular endothelium and are thought to cause endothelial dysfunction and to contribute to the development of hypertension during pregnancy. Due to the difficulty in studying such soluble factors in pregnant women, various animal models have been designed. Studies from these models have contributed to a better understanding of how factors released in response to placental ischemia may lead to increased blood pressure and reduced fetal weight during pregnancy. This review will highlight various animal models and the major findings indicating the importance of placental ischemia to lead to the pathophysiology observed in preeclamptic patients.
authors.affiliation: Departments of Pharmacology, Physiology, & Ob/Gyn, Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, Jackson, MS, 39216, USA. bblamarca@umc.edu.
authors.forename: Babbette
authors.initials: B
authors.lastname: LaMarca
authors.affiliation: Departments of Pharmacology, Physiology, & Ob/Gyn, Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
authors.forename: Lorena M
authors.initials: LM
authors.lastname: Amaral
authors.affiliation: Departments of Pharmacology, Physiology, & Ob/Gyn, Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
authors.forename: Ashlyn C
authors.initials: AC
authors.lastname: Harmon
authors.affiliation: Departments of Pharmacology, Physiology, & Ob/Gyn, Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
authors.forename: Denise C
authors.initials: DC
authors.lastname: Cornelius
authors.affiliation: Departments of Pharmacology, Physiology, & Ob/Gyn, Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
authors.forename: Jessica L
authors.initials: JL
authors.lastname: Faulkner
authors.affiliation: Departments of Pharmacology, Physiology, & Ob/Gyn, Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
authors.forename: Mark W
authors.initials: MW
authors.lastname: Cunningham
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D046110:Hypertension, Pregnancy-Induced / Q000503:physiopathology*; D007511:Ischemia / Q000503:physiopathology*; D010641:Phenotype; D010920:Placenta / Q000098:blood supply / Q000503:physiopathology*; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D013601:T-Lymphocytes / Q000276:immunology
keywords: Animal models; Hypertension; Inflammation; Preeclampsia; Pregnancy