|
|||||
|
|
Epigenetic insight into effects of prenatal alcohol exposure on stress axis development: Systematic review with meta-analytic approaches |
|
| Authors: | Ujjal Das Omkaram Gangisetty Shaista Chaudhary Prashant Tarale Bénédicte Rousseau Julianne Price Ian Frazier Dipak K. Sarkar |
| Affiliation: | 1. Endocrinology Program, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, USA Department of Animal Sciences, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA;2. Molecular Neuroscience of Alcohol and Drug Abuse Research Training, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA;3. Molecular Neuroscience of Alcohol and Drug Abuse Research Training, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA Center of Alcohol & Substance Use Studies, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA Department of Kinesiology & Health, Rutgers, The State University of New Jersey, Piscataway, New Jersey, USA;4. Endocrinology Program, Rutgers, The State University of New Jersey, New Brunswick, New Jersey, USA |
| Abstract: | We conducted a systematic review with meta-analytic elements using publicly available Gene Expression Omnibus (GEO) datasets to determine the role of epigenetic mechanisms in prenatal alcohol exposure (PAE)-induced hypothalamic–pituitary–adrenal (HPA) axis dysfunctions in offspring. Several studies have demonstrated that PAE has long-term consequences on HPA axis functions in offspring. Some studies determined that alcohol-induced epigenetic alterations during fetal development persist in adulthood. However, additional research is needed to understand the major epigenetic events leading to alcohol-induced teratogenesis of the HPA axis. Our network analysis of GEO datasets identified key pathways relevant to alcohol-mediated histone modifications, DNA methylation, and miRNA involvement associated with PAE-induced alterations of the HPA axis. Our analysis indicated that PAE perturbated the epigenetic machinery to activate corticotrophin-releasing hormone, while it suppressed opioid, glucocorticoid receptor, and circadian clock genes. These results help to further our understanding of the epigenetic basis of alcohol's effects on HPA axis development. |
| Keywords: | epigenetic fetal alcohol stress axis |