Location: Reproduction ResearchTitle: Development of the Pig Placenta) Author
Submitted to: Reproduction and Fertility Supplement
Publication Type: Review Article
Publication Acceptance Date: 4/27/2009
Publication Date: 7/20/2009
Publication URL: handle.nal.usda.gov/10113/42275
Citation: Vallet, J.L., Miles, J.R., Freking, B.A. 2009. Development of the Pig Placenta. IN: Control of Pig Reproduction VIII (Rodriguez-Martinez, H., Vallet, J.L., Ziecik, A.J., eds.), Nottingham University Press. Proceedings of the Eighth International Conference on Pig Reproduction, May 31-June 4, 2009, The Banff Centre, Banff, Alberta, Canada. Society of Reproduction and Fertility Supplement. 66:265-279. Interpretive Summary: The number of piglets weaned per sow in a year has a large influence on the profitability of swine production. Deficits in placental function during pregnancy influence the number of piglets weaned by affecting the number of fully-formed piglets at birth, the stillbirth rate, and preweaning mortality, primarily by reduction of the delivery of the substrates needed for adequate fetal growth. This report reviews the factors known or suspected to influence pig placental development and the efficiency of transport of various substrates required for fetal development during pregnancy including some of our own previously published work and recently generated unpublished research results. It is intentionally broad and covers the contribution to placental development of the process of conceptus elongation during early pregnancy, placental structural development during later pregnancy, placental angiogenesis, and substrate-specific mechanisms of the pig placenta that contribute to substrate delivery to the developing pig fetus. A number of useful avenues for future research are indicated regarding each of these topics. Among these, the generation of high fructose concentrations by the pig placenta is enigmatic because use of fructose by the pig fetus for energy may be limited. Further understanding of the role of fructose and of the control of the other factors affecting placental development and function during pregnancy will lead to strategies to increase the number of piglets weaned per sow in a year.
Technical Abstract: Placental insufficiency results in a myriad of negative consequences, including death of the fetus or low birth weight of the piglet, which increases the risk of stillbirth, preweaning mortality, and poor growth potential. Placental function is controlled by the size of the placenta, its structural characteristics relevant to maternal-fetal exchange of nutrients, and specialized mechanisms that are specific to individual nutrients. Placental development begins at conceptus elongation. Elongation in relation to littermates is likely to be a primary factor controlling the size of the placenta and the uterine space available to each conceptus. After elongation, the allantois develops outward from the embryo to establish the allantochorionic placenta. The extent of growth of the allantois also contributes to the size of the functional placenta. During implantation in the pig, chorionic trophoblast cells become adhered to endometrial cells without erosion of either cell layer. Between day 30 and 35 of gestation, the adhered trophoblast-endometrial epithelial bilayer undergoes microscopic folding. Fetal and maternal capillaries develop on either side of this boundary and blood flows of each are arranged in a cross-countercurrent manner. The folds and capillaries represent the structural units of the pig placenta that are relevant to function. In addition, placental structures known as areolae develop from trophoblast at the mouths of the endometrial glands and take up endometrial gland secreted products (histotroph). By day 85, the microscopic folds deepen and secondary folds begin to develop. The epithelial bilayer also becomes thinner and capillaries invade the plane of each epithelial layer (but do not penetrate it) so that the distance between maternal and fetal capillaries is reduced. The folded bilayer is embedded in placental stromal tissue, which is partially composed of glycosaminoglycans, the most abundant being hyaluronan and heparan sulfate. Changes in both hyaluronoglucosaminidase and heparanase enzymes during placental development suggest that these enzymes play a role in placental structural development and capillary formation. In addition to these structural modifications, various nutrient specific transport mechanisms exist. Where they exist, nutrient-specific mechanisms are likely to be as important an influence on transport of that nutrient as placental size or structure. Our challenge is to understand placental development and function in sufficient detail to improve the transport of the most limiting nutrients to the developing pig fetus.