Uteroplacental vascular development and placental function: an update

Abstract

The importance of the placenta and its vascular development to fetal growth and development has been appreciated since ancient times. Based on numerous studies in humans and animal model organisms in the last 2-3 decades, normal placental angiogenesis is critically important to ensure adequate blood flow to the placenta and therefore to provide the substrates that support normal fetal growth. Placental angiogenesis is abnormal at term in compromised pregnancies (those in which fetal growth is altered), including those resulting from maternal nutritional or environmental stress, maternal age, increased numbers of fetuses, maternal or fetal genotype, or the use of assisted reproductive technologies (e.g., cloning by somatic cell nuclear transfer). We and others have recently shown that these defects in placental vascular development occur quite early in pregnancy and may therefore presage compromised fetal growth and development. The challenges will be to find biomarkers of abnormal placental angiogenesis and to develop therapeutic strategies to "rescue" placental vascular development and thus fetal growth in compromised pregnancies. Animal models will be essential in meeting these challenges.

Maternal backfat depth in gestating sows has a greater influence on offspring growth and carcass lean yield than maternal feed allocation during gestation

“…IGF-1 can induce nitric oxide production in endothelial cells. Nitric oxide functions as an endogenous vasodilator (Tsukahara et al, 1994) resulting in higher blood flow to the placenta, thereby increasing nutrient availability to the foetus (Reynolds et al, 2010). Therefore, the fact that Restricted gilts with low IGF-1 concentrations gave birth to the lightest piglets (Amdi et al, 2013), may not simply be a result of restricted nutrient supply but also due to decreased blood flow across the placenta.…”

Placental development during early pregnancy in sheep: vascular growth and expression of angiogenic factors in maternal placenta

“…These are astonishing figures, and highlight the early part of pregnancy as a critical period of pregnancy, which is not surprising as this is the time during which embryonic organogenesis occurs and the placenta is established (Reynolds et al 2010). High embryonic loss may appear as a consequence of a variety of negative effects, and thus establishes the need to analyze angiogenesis in both normal and compromised pregnancies, such as those generated from assisted reproductive technologies, or affected by environmental factors such as malnutrition or other factors leading to stress.…”

“…Inadequate vascular growth during early pregnancy may be associated with inadequate uterine and umbilical blood flow, which directly affects transport of nutrients to the embryo/fetus. The consequences of inadequate placental vascular development include compromised implantation, spontaneous abortion/ embryonic loss, defective formation of the placenta, and altered fetal growth and development resulting in intrauterine growth restriction potentially leading to reduced lifelong health and productivity of the offspring (Sherer & Abulafia 2001, Wallace et al 2002, Torry et al 2004, Reynolds et al 2005a, 2005b, 2005c, 2010, Demir et al 2007.…”

“…Angiogenesis is the formation of new blood vessels from pre-existing vasculature, and it is a critical process for the growth and development of all tissues, including the placenta (Reynolds & Redmer 1992, 1998, Borowicz et al 2007, Reynolds et al 2010. Growth of the tissue is associated with the high metabolic demands (Reynolds & Redmer 1998).…”

“…The placenta, which serves as the organ of exchange between maternal and fetal systems, represents a very fast growing tissue with a high metabolic demand that requires a dynamic angiogenic process from early to late pregnancy to support its growth and function (Reynolds & Redmer 1995, Mayhew 2002, Redmer et al 2004, Torry et al 2004, Reynolds et al 2005a, 2005b, 2005c, 2010. Angiogenesis is regulated by numerous angiogenic and other factors including vascular endothelial growth factor (VEGF) family, fibroblast growth factor 2 (FGF2, also known as basic FGF), angiopoietins (ANGPT), nitric oxide (NO), and other systems (Reynolds & Redmer 1998, Reynolds et al 2005a, 2005b, 2005c, 2010. Moreover, in compromised pregnancies (that is, pregnancies in which fetal or placental growth, or both, is affected), placental angiogenesis is also abnormal at mid to late periods , Reynolds et al 2005a, 2005b, 2005c, 2010, Burton et al 2009).…”