Format

Send to

Choose Destination
Epigenetics. 2014 Jan;9(1):81-9. doi: 10.4161/epi.26197. Epub 2013 Sep 30.

Imprinted and X-linked non-coding RNAs as potential regulators of human placental function.

Author information

1
The Robinson Institute; Research Centre for Reproductive Health; School of Paediatrics and Reproductive Health; The University of Adelaide; Adelaide, SA Australia.
2
The Robinson Institute; Research Centre for Reproductive Health; School of Paediatrics and Reproductive Health; The University of Adelaide; Adelaide, SA Australia; School of Agriculture Food & Wine; The University of Adelaide; Adelaide, SA Australia.

Abstract

Pregnancy outcome is inextricably linked to placental development, which is strictly controlled temporally and spatially through mechanisms that are only partially understood. However, increasing evidence suggests non-coding RNAs (ncRNAs) direct and regulate a considerable number of biological processes and therefore may constitute a previously hidden layer of regulatory information in the placenta. Many ncRNAs, including both microRNAs and long non-coding transcripts, show almost exclusive or predominant expression in the placenta compared with other somatic tissues and display altered expression patterns in placentas from complicated pregnancies. In this review, we explore the results of recent genome-scale and single gene expression studies using human placental tissue, but include studies in the mouse where human data are lacking. Our review focuses on the ncRNAs epigenetically regulated through genomic imprinting or X-chromosome inactivation and includes recent evidence surrounding the H19 lincRNA, the imprinted C19MC cluster microRNAs, and X-linked miRNAs associated with pregnancy complications.

KEYWORDS:

epigenetics; microRNA; non-coding RNA; placenta; preeclampsia; pregnancy

PMID:
24081302
PMCID:
PMC3928189
DOI:
10.4161/epi.26197
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Taylor & Francis Icon for PubMed Central
Loading ...
Support Center