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      Epigenetic Modifications of Major Depressive Disorder

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          Abstract

          Major depressive disorder (MDD) is a chronic disease whose neurological basis and pathophysiology remain poorly understood. Initially, it was proposed that genetic variations were responsible for the development of this disease. Nevertheless, several studies within the last decade have provided evidence suggesting that environmental factors play an important role in MDD pathophysiology. Alterations in epigenetics mechanism, such as DNA methylation, histone modification and microRNA expression could favor MDD advance in response to stressful experiences and environmental factors. The aim of this review is to describe genetic alterations, and particularly altered epigenetic mechanisms, that could be determinants for MDD progress, and how these alterations may arise as useful screening, diagnosis and treatment monitoring biomarkers of depressive disorders.

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          Origins and Mechanisms of miRNAs and siRNAs.

          Richard W. Carthew, Erik J. Sontheimer (2009)
          Over the last decade, approximately 20-30 nucleotide RNA molecules have emerged as critical regulators in the expression and function of eukaryotic genomes. Two primary categories of these small RNAs--short interfering RNAs (siRNAs) and microRNAs (miRNAs)--act in both somatic and germline lineages in a broad range of eukaryotic species to regulate endogenous genes and to defend the genome from invasive nucleic acids. Recent advances have revealed unexpected diversity in their biogenesis pathways and the regulatory mechanisms that they access. Our understanding of siRNA- and miRNA-based regulation has direct implications for fundamental biology as well as disease etiology and treatment.
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            Epigenetic programming by maternal behavior.

            Ian Weaver, Nadia Cervoni, Frances Champagne … (2004)
            Here we report that increased pup licking and grooming (LG) and arched-back nursing (ABN) by rat mothers altered the offspring epigenome at a glucocorticoid receptor (GR) gene promoter in the hippocampus. Offspring of mothers that showed high levels of LG and ABN were found to have differences in DNA methylation, as compared to offspring of 'low-LG-ABN' mothers. These differences emerged over the first week of life, were reversed with cross-fostering, persisted into adulthood and were associated with altered histone acetylation and transcription factor (NGFI-A) binding to the GR promoter. Central infusion of a histone deacetylase inhibitor removed the group differences in histone acetylation, DNA methylation, NGFI-A binding, GR expression and hypothalamic-pituitary-adrenal (HPA) responses to stress, suggesting a causal relation among epigenomic state, GR expression and the maternal effect on stress responses in the offspring. Thus we show that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible.
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              Sustained hippocampal chromatin regulation in a mouse model of depression and antidepressant action.

              Nadia Tsankova, Olivier Berton, William Renthal … (2006)
              To better understand the molecular mechanisms of depression and antidepressant action, we administered chronic social defeat stress followed by chronic imipramine (a tricyclic antidepressant) to mice and studied adaptations at the levels of gene expression and chromatin remodeling of five brain-derived neurotrophic factor (Bdnf) splice variant mRNAs (I-V) and their unique promoters in the hippocampus. Defeat stress induced lasting downregulation of Bdnf transcripts III and IV and robustly increased repressive histone methylation at their corresponding promoters. Chronic imipramine reversed this downregulation and increased histone acetylation at these promoters. This hyperacetylation by chronic imipramine was associated with a selective downregulation of histone deacetylase (Hdac) 5. Furthermore, viral-mediated HDAC5 overexpression in the hippocampus blocked imipramine's ability to reverse depression-like behavior. These experiments underscore an important role for histone remodeling in the pathophysiology and treatment of depression and highlight the therapeutic potential for histone methylation and deacetylation inhibitors in depression.
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                Author and article information

                Contributors
                Stephen A. Bustin: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 05 August 2016
                Publication date Collection: August 2016
                Volume: 17
                Issue: 8
                Electronic Location Identifier: 1279
                Affiliations
                [1 ]Center of Molecular Biology and Pharmacogenetics, Scientific and Technological Bioresource Nucleus, Universidad de La Frontera, Temuco 4811230, Chile; kathleen.saavedra@ 123456ufrontera.cl (K.S.); anamariamolinamarquez@ 123456gmail.com (A.M.M.-M.); nicolas.saavedra@ 123456ufrontera.cl (N.S.); tomas.zambrano@ 123456ufrontera.cl (T.Z.)
                [2 ]Millennium Institute for Research in Depression and Personality (MIDAP), Universidad de La Frontera, Temuco 4811230, Chile
                Author notes
                [* ]Correspondence: luis.salazar@ 123456ufrontera.cl ; Tel.: +56-45-259-6724
                Article
                Publisher ID: ijms-17-01279
                DOI: 10.3390/ijms17081279
                PMC ID: 5000676
                PubMed ID: 27527165
                SO-VID: c409037b-ca58-49ee-b451-fcef86716c3d
                Copyright © © 2016 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 20 June 2016
                Date accepted : 29 July 2016
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: major depressive disorder,depression,epigenetic modifications,methylation,histone modification,mirnas,biomarkers
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: major depressive disorder, depression, epigenetic modifications, methylation, histone modification, mirnas, biomarkers

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