title: Placental growth, angiogenic gene expression, and vascular development in undernourished adolescent sheep.
abstract: Limiting maternal nutrient intake during ovine adolescent pregnancy progressively depleted maternal body reserves, impaired fetal nutrient supply, and slowed fetal soft tissue growth. The present study examined placental growth, angiogenic gene expression, and vascular development in this undernourished adolescent model at Days 90 and 130 of gestation. Singleton pregnancies were established, and ewes were offered an optimal control (C; n = 14) or low (L [0.7 x C]; n = 21) dietary intake. Seven ewes receiving L intakes were switched to C intakes on Day 90 of gestation (L-C). Fetal body weight (P < 0.01) and glucose concentrations (P < 0.03) were reduced in L versus C pregnancies by Day 130, whereas L-C group values were intermediate. Placental cellular proliferation, gross morphology, and mass were independent of maternal nutrition at both Day 90 and 130. In contrast, capillary area density in the maternal caruncular portion of the placentome was reduced by 20% (P < 0.001) at both stages of gestation in L compared with C groups. Caruncular capillary area density was equivalent in the L and L-C groups at Day 130. Placental mRNA expression of five key angiogenic ligands or receptors increased (P < 0.001) between Days 90 and 130 of gestation. VEGFA mRNA expression was higher (P < 0.04) in L compared with C and L-C pregnancies at Day 130, but otherwise gene expression of the remaining angiogenic factors and receptors analyzed was unaffected by maternal intake. Undernourishing the pregnant adolescent dam restricts fetal growth independently of changes in placental mass. Alterations in maternal placental vascular development may, however, play a role in mediating the previously reported reduction in maternal and hence fetal nutrient supply.
authors.affiliation: Rowett Research Institute, Bucksburn, Aberdeen AB21 9SB, United Kingdom.
authors.forename: Justin
authors.initials: J
authors.lastname: Luther
authors.forename: John
authors.initials: J
authors.lastname: Milne
authors.forename: Raymond
authors.initials: R
authors.lastname: Aitken
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Matsuzaki
authors.forename: Lawrence
authors.initials: L
authors.lastname: Reynolds
authors.forename: Dale
authors.initials: D
authors.lastname: Redmer
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Wallace
mesh_terms: D042501:Angiogenic Proteins / Q000235:genetics; D000818:Animals; D004032:Diet; D005260:Female; D047109:Fetal Development; D020567:Fetal Weight; D015870:Gene Expression; D005865:Gestational Age; D044342:Malnutrition / Q000503:physiopathology / Q000662:veterinary*; D018919:Neovascularization, Physiologic / Q000235:genetics* / Q000502:physiology; D010920:Placenta / Q000098:blood supply* / Q000737:chemistry; D010929:Placentation; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology / Q000662:veterinary*; D012333:RNA, Messenger / Q000032:analysis; D040262:Receptors, Vascular Endothelial Growth Factor / Q000235:genetics; D012756:Sheep; D012757:Sheep Diseases / Q000503:physiopathology*; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics
chemical_list: D042501:Angiogenic Proteins; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D040262:Receptors, Vascular Endothelial Growth Factor