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Bioscientifica Proceedings (2020) 18 CPRCPR31 | DOI: 10.1530/biosciprocs.18.0031

USDA, ARS, U.S. Meat Animal Research Center, P. 0. Box 166, State Spur 18D, Clay Center, Nebraska 68933, USA

Placental insufficiency results in fetal loss, low birth weight, stillbirth, preweaning mortality and poor growth. Placental development begins at conceptus elongation, which is a primary factor controlling the size of the placenta. After elongation, the allantois develops outward from the embryo to establish the al lantochorion, which defines the size of the functional placenta. During implantation, chorionic trophoblasts adhere to endometrial epithelial cells. Placental structures known as areolae develop at the openings of the endometrial glands and take up endometrial gland secreted products (histotrophe). Between day 30 and 35 of gestation, the adhered trophoblast-endometrial epithelial bi layer undergoes microscopic folding. Fetal and maternal capillaries develop adjacent to the bilayer and blood flows are arranged in a cross-countercurrent manner. Except for nutrients secreted by the glands, nutrient exchange takes place between these capillaries within these folds. By day 85, the folds deepen and become more complex, increasing surface area. The epithelial bilayer thins and capillaries indent the plane of each layer (but do not penetrate), reducing distance between capillaries. The folded bilayer is surrounded by endometrial stroma on the maternal side and placental stroma on the fetal side. The fetal-placental stroma is partially composed of glycosaminoglycans, the most abundant being hyaluronan and heparan sulfate. Changes in both hyaluronoglucosaminidase and heparanase during placental development suggest that these enzymes play a role in placental development. In addition to structural modifications, various nutrient specific transport mechanisms exist. These mechanisms are likely to be as important to transport of specific nutrients as placental size or structure.

© 2009 Society for Reproduction and Fertility

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