Epigenetic regulation of placental endocrine lineages and complications of pregnancy

John, Rosalind Margaret ORCID: https://orcid.org/0000-0002-3827-7617 2013. Epigenetic regulation of placental endocrine lineages and complications of pregnancy. Biochemical Society Transactions 41 (3) , pp. 701-709. 10.1042/BST20130002

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Abstract

A defining feature of mammals is the development in utero of the fetus supported by the constant flow of nutrients from the mother obtained via a specialized organ: the placenta. The placenta is also a major endocrine organ that synthesizes vast quantities of hormones and cytokines to instruct both maternal and fetal physiology. Nearly 20 years ago, David Haig and colleagues proposed that placental hormones were likely targets of the epigenetic process of genomic imprinting in response to the genetic conflicts imposed by in utero development [Haig (1993) Q. Rev. Biol. 68, 495–532]. There are two simple mechanisms through which genomic imprinting could regulate placental hormones. First, imprints could directly switch on or off alleles of specific genes. Secondly, imprinted genes could alter the expression of placental hormones by regulating the development of placental endocrine lineages. In mice, the placental hormones are synthesized in the trophoblast giant cells and spongiotrophoblast cells of the mature placenta. In the present article, I review the functional role of imprinted genes in regulating these endocrine lineages, which lends support to Haig's original hypothesis. I also discuss how imprinting defects in the placenta may adversely affect the health of the fetus and its mother during pregnancy and beyond.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Subjects:	Q Science > QH Natural history > QH426 Genetics Q Science > QP Physiology R Medicine > RG Gynecology and obstetrics
Publisher:	Biochemical Society
ISSN:	0300-5127
Funders:	BBSRC
Last Modified:	24 Oct 2022 11:58
URI:	https://orca.cardiff.ac.uk/id/eprint/49898

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