Preeclampsia as a parental epigenetic disease

Abstract

Objectives: Preeclampsia still remains a major cause of maternal and perinatal mortality and morbidity. The aim of this study is to provide an overview of the evidence from epigenetic regulation of preeclampsia development, with a focus on candidate imprinted genes and their roles. Materials and Methods: A PubMed search of the relevant literature published between 2005 and 2016 was performed to identify the preeclampsia susceptibility genes and imprinted genes. Results: Several susceptibility genes that have highlighted the potential role of preeclampsia development have been identified. There appears to be at least two types of genes in the placenta: the paternity-related genes appear to be evolved as the trophoblast invasion and fetal growth, while the maternity-related genes act as the defence and protective mechanism for the mother. A number of imprinting genes are essential for the biological functions such as decidualization, pregnancy maintenance, tumor suppressor, and fetal developmental processes, which include paternally expressed/maternally imprinted genes and maternally expressed/paternally imprinted genes. Some biological aspects of preeclampsia are explained from an imbalanced expression of genomic imprinting (epigenetic conflict). Although the genotypic and phenotypic extent of multilocus imprinting epimutations is poorly understood, the preeclamptic placenta showed unique epigenetic features. Changes of parental life experiences with stress or early-life conditions during pregnancy may display impaired reproductive outcome through the dynamic alterations in the patterns of the specific imprinted genes. Conclusion: In conclusion, preeclampsia may be recognized as a parental imprinting disease.