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UNSW Embryology

Placenta Development - Vascular Beds

© Dr Mark Hill (2008)

Acknowledgements

Introduction

This page gives an overview of placental circulation based upon a recent paper on the molecular regulation of mouse placenta development. (More? Mouse Development)

These resin casts are generated by filling the existing vascular beds (day 16.5 p.c.) with a resin that sets and the surrounding materials are then removed, leaving just the vascular beds. Venous side (red resin) and arterial side (blue resin).

Placenta Superior View

Placenta Lateral View

Placenta lateral view

Reference

Rodriguez TA, Sparrow DB, Scott AN, Withington SL, Preis JI, Michalicek J, Clements M, Tsang TE, Shioda T, Beddington RS, Dunwoodie SL.    [See Related Articles] Cited1 is required in trophoblasts for placental development and for embryo growth and survival. Mol Cell Biol. 2004 Jan;24(1):228-44.

"Cited1 is a transcriptional cofactor that interacts with Smad4, estrogen receptors alpha and beta, TFAP2, and CBP/p300. It is expressed in a restricted manner in the embryo as well as in extraembryonic tissues during embryonic development. In this study we report the engineering of a loss-of-function Cited1 mutation in the mouse. Cited1 null mutants show growth restriction at 18.5 days postcoitum, and most of them die shortly after birth. Half the heterozygous females, i.e., those that carry a paternally inherited wild-type Cited1 allele, are similarly affected. Cited1 is normally expressed in trophectoderm-derived c ells of the placenta; however, in these heterozygous females, Cited1 is not expressed in these cells. This occurs because Cited1 is located on the X chromosome, and thus the wild-type Cited1 allele is not expressed because the paternal X chromosome is preferentially inactivated. Loss of Cited1 resulted in abnormal placental development. In mutants, the spongiotrophoblast layer is irregular in shape and enlarged while the labyrinthine layer is reduced in size. In addition, the blood spaces within the labyrinthine layer are disrupted; the maternal sinusoids are considerably larger in mutants, leading to a reduction in the surface area available for nutrient exchange. We conclude that Cited1 is required in trophoblasts for normal placental development and subsequently for embryo viability."

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