Birthweight is associated with DNA promoter methylation of the glucocorticoid receptor in human placenta

Birthweight has been associated with a number of health outcomes throughout life. Crucial to proper infant growth and development is the placenta, and alterations to placental gene function may reflect differences in the intrauterine environment which functionally contribute to infant growth and may...

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Bibliographic Details
Published in:Epigenetics 2011-05, Vol.6 (5), p.566-572
Main Authors: Filiberto, Amanda C, Maccani, Matthew A, Koestler, Devin, Wilhelm-Benartzi, Charlotte, Avissar-Whiting, Michele, Banister, Carolyn E, Gagne, Luc A, Marsit, Carmen J
Format: Article
Language:English
Subjects:
Binding
Biology
Bioscience
Birth Weight - genetics
Brief
Calcium
Cancer
Cell
Cycle
DNA Methylation - genetics
Epigenesis, Genetic
Exons
Female
Humans
Infant, Newborn
Landes
Male
Organogenesis
Placenta - metabolism
Pregnancy
Promoter Regions, Genetic
Proteins
Receptors, Glucocorticoid - genetics
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Summary:Birthweight has been associated with a number of health outcomes throughout life. Crucial to proper infant growth and development is the placenta, and alterations to placental gene function may reflect differences in the intrauterine environment which functionally contribute to infant growth and may ultimately affect the child’s health. To examine if epigenetic alteration to the glucocorticoid receptor (GR) gene was linked to infant growth, we analyzed 480 human placentas for differential methylation of the GR gene exon 1F and examined how this variation in methylation extent was associated with fetal growth. Multivariable linear regression revealed a significant association (p < 0.0001) between differential methylation of the GR gene and large for gestational age (LGA) status. Our work is one of the first to link infant growth as a measure of the intrauterine environment and epigenetic alterations to the GR and suggests that DNA methylation may be a critical determinant of placental function.
ISSN:1559-2294
1559-2308
DOI:10.4161/epi.6.5.15236