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Special Issue "Epigenetic Regulation in Human Brain"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 April 2021).

Special Issue Editor

Dr. Alexey Kozlenkov
E-Mail
Guest Editor
Icahn School of Medicine at Mount Sinai, New York, United States
Interests: neurobiology; epigenetics; molecular biology; DNA methylation; DNA hydroxymethylaion; neuropsychiatric disorders; flow cytometry; high-throughput sequencing

Special Issue Information

Dear Colleagues, 

The human brain is an organ of enormous complexity, composed of a multitude of cell types, including various populations of neuronal and glial cells. Epigenetics has been recognized for a long time as a group of molecular mechanisms that are essential in establishing and maintaining this complexity. Understanding the epigenetics of brain cell types is also necessary to uncover the mechanisms underlying nervous system disorders, which often display cell type-specific aetiology. However, in recent years, a number of methodological advances have allowed us to study brain epigenetics at cell-type resolution for the first time and brought the recognition of often vast and unexpected differences between the epigenomic profiles of brain cell populations. Despite this fast and promising progress, the field is currently wide open for new insights and discoveries, especially in the studies of brain development, disease, and ageing. A significantly more thorough understanding of neuroepigenetic mechanisms is also needed before we can efficiently transfer this line of research to the stage of therapeutic opportunities. In this Special Issue, we will highlight modern developments in the field of neuroepigenetics of human brain cell populations, in its relationship to brain development, health, and disease.

Dr. Alexey Kozlenkov
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • epigenetics
  • DNA methylation
  • histone modifications
  • human brain
  • neurons
  • glutamatergic neurons
  • glia

Published Papers (2 papers)

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Research

Open AccessArticle
Epigenetic Consequences of in Utero Exposure to Rosuvastatin: Alteration of Histone Methylation Patterns in Newborn Rat Brains
Int. J. Mol. Sci. 2021, 22(7), 3412; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073412 - 26 Mar 2021
Viewed by 335
Abstract
Rosuvastatin (RST) is primarily used to treat high cholesterol levels. As it has potentially harmful but not well-documented effects on embryos, RST is contraindicated during pregnancy. To demonstrate whether RST could induce molecular epigenetic events in the brains of newborn rats, pregnant mothers [...] Read more.
Rosuvastatin (RST) is primarily used to treat high cholesterol levels. As it has potentially harmful but not well-documented effects on embryos, RST is contraindicated during pregnancy. To demonstrate whether RST could induce molecular epigenetic events in the brains of newborn rats, pregnant mothers were treated daily with oral RST from the 11th day of pregnancy for 10 days (or until delivery). On postnatal day 1, the brains of the control and RST-treated rats were removed for Western blot or immunohistochemical analyses. Several antibodies that recognize different methylation sites for H2A, H2B, H3, and H4 histones were quantified. Analyses of cell-type-specific markers in the newborn brains demonstrated that prenatal RST administration did not affect the composition and cell type ratios as compared to the controls. Prenatal RST administration did, however, induce a general, nonsignificant increase in H2AK118me1, H2BK5me1, H3, H3K9me3, H3K27me3, H3K36me2, H4, H4K20me2, and H4K20me3 levels, compared to the controls. Moreover, significant changes were detected in the number of H3K4me1 and H3K4me3 sites (134.3% ± 19.2% and 127.8% ± 8.5% of the controls, respectively), which are generally recognized as transcriptional activators. Fluorescent/confocal immunohistochemistry for cell-type-specific markers and histone methylation marks on tissue sections indicated that most of the increase at these sites belonged to neuronal cell nuclei. Thus, prenatal RST treatment induces epigenetic changes that could affect neuronal differentiation and development. Full article
(This article belongs to the Special Issue Epigenetic Regulation in Human Brain)
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Open AccessArticle
Downregulation of the Polycomb-Associated Methyltransferase Ezh2 during Maturation of Hippocampal Neurons Is Mediated by MicroRNAs Let-7 and miR-124
Int. J. Mol. Sci. 2020, 21(22), 8472; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228472 - 11 Nov 2020
Cited by 1 | Viewed by 534
Abstract
Ezh2 is a catalytic subunit of the polycomb repressive complex 2 (PRC2) which mediates epigenetic gene silencing through depositing the mark histone H3 lysine 27 trimethylation (H3K27me3) at target genomic sequences. Previous studies have demonstrated that Enhancer of Zeste Homolog 2 (Ezh2) was [...] Read more.
Ezh2 is a catalytic subunit of the polycomb repressive complex 2 (PRC2) which mediates epigenetic gene silencing through depositing the mark histone H3 lysine 27 trimethylation (H3K27me3) at target genomic sequences. Previous studies have demonstrated that Enhancer of Zeste Homolog 2 (Ezh2) was differentially expressed during maturation of hippocampal neurons; in immature neurons, Ezh2 was abundantly expressed, whereas in mature neurons the expression Ezh2 was significantly reduced. Here, we report that Ezh2 is downregulated by microRNAs (miRs) that are expressed during the hippocampal maturation process. We show that, in mature hippocampal neurons, lethal-7 (let-7) and microRNA-124 (miR-124) are robustly expressed and can target cognate motifs at the 3′-UTR of the Ezh2 gene sequence to downregulate Ezh2 expression. Together, these data demonstrate that the PRC2 repressive activity during hippocampal maturation is controlled through a post-transcriptional mechanism that mediates Ezh2 downregulation in mature neurons. Full article
(This article belongs to the Special Issue Epigenetic Regulation in Human Brain)
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