Epigenetic programming of hypoxic-ischemic encephalopathy in response to fetal hypoxia

Authors

Qingyi Ma, Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.Follow
Lubo Zhang, Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.Follow

Document Type

Article

Publication Date

1-1-2015

Publication Title

Progress in neurobiology

E-ISSN

1873-5118

Abstract

Hypoxia is a major stress to the fetal development and may result in irreversible injury in the developing brain, increased risk of central nervous system (CNS) malformations in the neonatal brain and long-term neurological complications in offspring. Current evidence indicates that epigenetic mechanisms may contribute to the development of hypoxic/ischemic-sensitive phenotype in the developing brain in response to fetal stress. However, the causative cellular and molecular mechanisms remain elusive. In the present review, we summarize the recent findings of epigenetic mechanisms in the development of the brain and their roles in fetal hypoxia-induced brain developmental malformations. Specifically, we focus on DNA methylation and active demethylation, histone modifications and microRNAs in the regulation of neuronal and vascular developmental plasticity, which may play a role in fetal stress-induced epigenetic programming of hypoxic/ischemic-sensitive phenotype in the developing brain.

Volume

124

First Page

28

Last Page

48

DOI

10.1016/j.pneurobio.2014.11.001

PubMed ID

25450949

Recommended Citation

Ma, Qingyi and Zhang, Lubo, "Epigenetic programming of hypoxic-ischemic encephalopathy in response to fetal hypoxia" (2015). Loma Linda University Faculty Publications. 343.
https://scholarsrepository.llu.edu/fac_pubs/343