Supported by a grant from the National Institutes of Health (HD048510 to J.A.P.).
The role of imprinted genes in fetal growth abnormalities†
Article first published online: 6 JUN 2011
Copyright © 2011 Wiley-Liss, Inc.
Birth Defects Research Part A: Clinical and Molecular Teratology
Special Issue: Epigenetic Processes in Development
Volume 91, Issue 8, pages 682–692, August 2011
How to Cite
Piedrahita, J. A. (2011), The role of imprinted genes in fetal growth abnormalities. Birth Defects Research Part A: Clinical and Molecular Teratology, 91: 682–692. doi: 10.1002/bdra.20795
- Issue published online: 5 AUG 2011
- Article first published online: 6 JUN 2011
- Manuscript Accepted: 26 JAN 2011
- Manuscript Revised: 13 DEC 2010
- Manuscript Received: 15 NOV 2010
- National Institutes of Health. Grant Number: HD048510
Epigenetics, and in particular imprinted genes, have a critical role in the development and function of the placenta, which in turn has a central role in the regulation of fetal growth and development. A unique characteristic of imprinted genes is their expression from only one allele, maternal or paternal and dependent on parent of origin. This unique expression pattern may have arisen as a mechanism to control the flow of nutrients from the mother to the fetus, with maternally expressed imprinted genes reducing the flow of resources and paternally expressed genes increasing resources to the fetus. As a result, any epigenetic deregulation affecting this balance can result in fetal growth abnormalities. Imprinting-associated disorders in humans, such as Beckwith-Wiedemann and Angelman syndrome, support the role of imprinted genes in fetal growth. Similarly, assisted reproductive technologies in animals have been shown to affect the epigenome of the early embryo and the expression of imprinted genes. Their role in disorders such as intrauterine growth restriction appears to be more complex, in that imprinted gene expression can be seen as both causative and protective of fetal growth restriction. This protective or compensatory effect needs to be explored more fully. © Birth Defects Research (Part A), 2011. © 2011 Wiley-Liss, Inc.