Associations Between Imprinted Gene Expression in the Placenta, Human Fetal Growth and Preeclampsia

Peer reviewed: 
Yes, item is peer reviewed.
Scholarly level: 
Faculty/Staff
Final version published as: 

Christians JK, Leavey K, Cox BJ. 2017.  Associations between imprinted gene expression in the placenta, human fetal growth and preeclampsia. Biology Letters. 13: 20170643. http://dx.doi.org/10.1098/rsbl.2017.0643

Date created: 
2017-11-29
Keywords: 
Placenta
Imprinting
Preeclampsia
Intrauterine growth restriction
Kinship theory
Abstract: 

Genomic imprinting is essential for normal placental and fetal growth. One theory to explain the evolution of imprinting is the kinship theory (KT), which predicts that genes that are paternally expressed will promote fetal growth, whereas maternally expressed genes will suppress growth. We investigated the expression of imprinted genes using microarray measurements of expression in term placentae. Correlations between birthweight and the expression levels of imprinted genes were more significant than for non-imprinted genes, but did not tend to be positive for paternally expressed genes and negative for maternally expressed genes.  Imprinted genes were more dysregulated in preeclampsia (a disorder associated with placental insufficiency) than randomly selected genes, and we observed an excess of patterns of dysregulation in preeclampsia that would be expected to reduce nutrient allocation to the fetus, given the predictions of the KT. However, we found no evidence of coordinated regulation among these imprinted genes. A few imprinted genes have previously been shown to be associated with fetal growth and preeclampsia, and our results indicate that this is true for a broader set of imprinted genes.

Description: 

The full text of this article will available December 2018 in accordance with the embargo policies of the Royal Society's publication Biology Letters. If you require access to the fulltext prior to December 2018 please contact summit@sfu.ca.

Language: 
English
Document type: 
Article
Rights: 
Rights remain with the authors.
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