The Biology of Non-Coding RNAs and Metabolic Diseases

A special issue of Non-Coding RNA (ISSN 2311-553X).

Deadline for manuscript submissions: closed (31 December 2016)

Special Issue Editors


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Guest Editor
Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia
Interests: diabetes; clinical and molecular epigenetics; chromatin; DNA and RNA methylation; histones; transcriptional regulation; computational epigenomics; metabolic disease
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Guest Editor
Department of Medicine & Therapeutics, The Chinese University of Hong Kong, 9/F, Lui Che Woo Clinical Sciences Building, Prince of Wales Hospital, Shatin, N.T., Hong Kong

Special Issue Information

Dear Colleagues,

Non-Coding RNA is now accepting submissions for a special issue on the biology of ncRNAs and metabolism and its disorders. The special issue is co-guest-edited by the Professor Assam El-Osta from the Baker IDI Heart & Diabetes Institute, and Professor Ronald Ma from The Chinese University of Hong Kong. This Special Issue will also include commissioned topical reviews written by leaders in the field. Accepted papers are published online immediately after copy editing.
Non-Coding RNA is an Open Access journal. There is no Article Processing Charges (APCs) for papers submitted in 2016.

The rising global epidemic of obesity, cardiovascular disease and diabetes underscores the current challenge of characterizing the metabolically responsive epigenome and understanding the role and interaction of ncRNAs. For example, studies in recent years investigating the molecular mechanisms linking fat and glucose metabolism with transcription highlight important regulatory determinants that underpin the expression of genes implicated in metabolic disease which are considered critical yet remain poorly understood. Together with the expression and interactions of ncRNAs, increasing evidence indicates that altered metabolism contributes to disease.

We will consider Research, Methods and Software manuscripts of exceptional interest on the following topics:

  • Discovery of ncRNAs implicated in metabolic health and disease
  • Overlap of epigenomics and ncRNAs in metabolism
  • Pre-clinical and clinical studies investigating metabolic or hyperglycemic memory
  • Integrative and multi-omic approaches to study metabolic disease
  • Population studies providing insights into ncRNAs
  • The use of ncRNAs and genomics in model organisms of metabolic disease
  • Connection between the nutritional environment of the developing fetus and ncRNA changes underlying pathological gene expression
  • Dietary factors conferring epigenetic or ncRNA changes associated with metabolic dysfunction
  • Resources of exceptional interest to the study of metabolism and its disorders

Prof. Dr. Assam El-Osta
Prof. Dr. Ronald Ma
Guest Editors

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 submissions that pass pre-check are 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. Non-Coding RNA is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). 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.

Published Papers (2 papers)

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Communication
Current perspectives in Set7 mediated stem cell differentiation
by Nazanin Karimnia, Haloom Rafehi, Natasha K Tuano, Mark Ziemann, Harikrishnan K.N, Jun Okabe and Assam El-Osta
Non-Coding RNA 2016, 2(4), 14; https://doi.org/10.3390/ncrna2040014 - 04 Dec 2016
Cited by 2 | Viewed by 5586
Abstract
Set7 is a key regulatory enzyme involved in the methylation of lysine residues of histone and non-histone proteins. This lysine methyltransferase is induced during stem cell differentiation and regulates lineage specific gene transcription and cell fate. In this article we discuss recent experimental [...] Read more.
Set7 is a key regulatory enzyme involved in the methylation of lysine residues of histone and non-histone proteins. This lysine methyltransferase is induced during stem cell differentiation and regulates lineage specific gene transcription and cell fate. In this article we discuss recent experimental evidence identifying regulatory targets under the control of Set7 as well as emerging evidence of regulation in stem cell differentiation. Furthermore, we discuss the function of non-coding RNAs regulated by Set7 implicated in cell plasticity. Full article
(This article belongs to the Special Issue The Biology of Non-Coding RNAs and Metabolic Diseases)
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Article
HDAC Inhibition in Vascular Endothelial Cells Regulates the Expression of ncRNAs
by Haloom Rafehi and Assam El-Osta
Non-Coding RNA 2016, 2(2), 4; https://doi.org/10.3390/ncrna2020004 - 25 May 2016
Cited by 14 | Viewed by 5432
Abstract
While clinical and pre-clinical trials indicate efficacy of histone deacetylase (HDAC) inhibitors in disease mediated by dynamic lysine modification, the impact on the expression of non-coding RNAs (ncRNAs) remains poorly understood. In this study, we investigate high throughput RNA sequencing data derived from [...] Read more.
While clinical and pre-clinical trials indicate efficacy of histone deacetylase (HDAC) inhibitors in disease mediated by dynamic lysine modification, the impact on the expression of non-coding RNAs (ncRNAs) remains poorly understood. In this study, we investigate high throughput RNA sequencing data derived from primary human endothelial cells stimulated with HDAC inhibitors suberanilohydroxamic acid (SAHA) and Trichostatin A (TSA). We observe robust regulation of ncRNA expression. Integration of gene expression data with histone 3 lysine 9 and 14 acetylation (H3K9/14ac) and histone 3 lysine 4 trimethylation (H3K4me3) datasets identified complex and class-specific expression of ncRNAs. We show that EP300 target genes are subject to histone deacetylation at their promoter following HDAC inhibition. This deacetylation drives suppression of protein-coding genes. However, long intergenic non-coding RNAs (lincRNAs) regulated by EP300 are activated following HDAC inhibition, despite histone deacetylation. This increased expression was driven by increased H3K4me3 at the gene promoter. For example, elevated promoter H3K4me3 increased lincRNA MALAT1 expression despite broad EP300-associated histone deacetylation. In conclusion, we show that HDAC inhibitors regulate the expression of ncRNA by complex and class-specific epigenetic mechanisms. Full article
(This article belongs to the Special Issue The Biology of Non-Coding RNAs and Metabolic Diseases)
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