Experimental manipulation of the rodent visceral yolk sac

Abstract

The visceral yolk sac (VYS) is an especially important placental organ in the rodent because it is the primary source of exchange between the embryo and mother during early organogenesis before the chorioallantoic placenta circulation is established. The VYS is involved with nutritional, endocrine, metabolic, immunologic, secretory, excretory, and hematopoietic functions. The VYS also plays a role in steroid metabolism and interacts with a variety of blood-borne factors: parathyroid hormone, glucocorticoids, insulin, and vitamin D metabolites. The importance of the VYS during development is emphasized by the embryotoxicity resulting from exposure to agents which cause VYS dysfunction when administered to the pregnant animal during organogenesis. Several experimental procedures have provided useful information concerning a variety of VYS functions from early organogenesis to term: Culture of the Embryo, Fetal Incubation, Culture of the Fetus, Giant Yolk Sac, Short- and Long-Term Culture of the Yolk Sac, Modified Ussing's Chamber, Single or Double Diffusion Chamber, and the use of Heterologous Rodent Visceral Yolk Sac Antibodies. Since human yolk sac pathology has been associated with developmental toxicity and spontaneous abortion, it is important to discover whether there are some common functional roles among different mammalian species and to determine if other experimental animal models can be used to study the possible contribution of human yolk sac dysfunction to some human reproductive problems.

Effect of dibutyltin on placental and fetal toxicity in rat

“…The yolk sac during this period plays a role as a transient placenta, and is the only route for major transport between dams and embryo until the formation of allantoic and the establishment of chorioallantoic placenta on GD 11 1/2 (Jollie, 1990). Impaired structural and functional development of the yolk sac contributes to the embryo toxicity and teratogenicity in rats (Beckman et al, 1990), such as trypan blue (Rogers et al, 1985) and ethanol (Xu et al, 2005). Therefore, the embryonic toxicity and teratogenicity during early post-implantation are induced not only by the direct effect of toxicant on the embryo damage directly but also by the secondary effect from dysfunction of the yolk sac placenta.…”

Disruption of the HNF-4 gene, expressed in visceral endoderm, leads to cell death in embryonic ectoderm and impaired gastrulation of mouse embryos.

“…By E5.5, the visceral endoderm forms a tight epithelial barrier around the rodent embryo medi ating exchange with external maternal blood and decid ual products (Parr and Parr 1986;Jollie 1990). The vis ceral endoderm later gives rise to the endodermal cells of the yolk sac; these cells are necessary for normal devel opment of rodent embryos as shown by the effects of exposure to various antivisceral endoderm agents (Beckman et al 1990). The yolk sac endoderm, like hepatocytes from which HNF-4 was originally isolated, is ac tive in secretion, transcytosis, and digestion (Jollie 1990).…”

The origin and evolution of genomic imprinting and viviparity in mammals

“…The rodent visceral yolk sac is also the route by which passive immunity (immunoglobulins) is passed to the embryo [24,25]. Agents that cause visceral yolk sac dysfunction during organogenesis can result in embryotoxicity and its damage leads to embryonic malformation [26]. In virtually all eutherian species studied, there is evidence of synthetic activity by the yolk sac and it serves as hematopoietic organ in all mammalian species studied (reviewed by King & Enders [22]).…”