Epigenetic Mechanisms in Diabetes Research

Editor


E-Mail Website
Collection 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
Special Issues, Collections and Topics in MDPI journals

Topical Collection Information

Dear Colleagues,

The rising global epidemic of obesity, cardiovascular disease and diabetes underscores the current challenge of characterizing the metabolically responsive epigenome. Recent studies investigating the molecular mechanisms linking fat and glucose metabolism with the epigenome highlight important regulatory determinants that underpin the expression of genes implicated in disease yet remain poorly understood. Epigenomes is now accepting submissions for a collection on "Epigenetic Mechanisms in Diabetes Research". This Topical Collection is edited by Professor Sam El-Osta from Monash University and will accept original research results and reviews, as well as special interest topics related to methods and resources of exceptional interest on topics related to metabolic regulation by epigenetic mechanisms in health and disease. You can find all the information related to the new Topical Collection at the following link: https://www.mdpi.com/journal/epigenomes/special_issues/diabetes.

We kindly invite you to submit your unpublished work to this Epigenomes Topical Collection, "Epigenetic Mechanisms in Diabetes Research".

I do hope you will join me in this Topical Collection.

Prof. Dr. Assam El-Osta
Collection 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 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 collection 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. Epigenomes is an international peer-reviewed open access quarterly 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 1500 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)

2024

Jump to: 2021

16 pages, 7042 KiB  
Article
Exploring Transcriptional Regulation of Beta Cell SASP by Brd4-Associated Proteins and Cell Cycle Control Protein p21
by Jasmine Manji, Jasmine Pipella, Gabriel Brawerman and Peter J. Thompson
Epigenomes 2024, 8(1), 10; https://doi.org/10.3390/epigenomes8010010 - 6 Mar 2024
Viewed by 1726
Abstract
Type 1 diabetes (T1D) is a metabolic disease resulting from progressive autoimmune destruction of insulin-producing pancreatic beta cells. Although the majority of beta cells are lost in T1D, a small subset undergoes senescence, a stress response involving growth arrest, DNA damage response, and [...] Read more.
Type 1 diabetes (T1D) is a metabolic disease resulting from progressive autoimmune destruction of insulin-producing pancreatic beta cells. Although the majority of beta cells are lost in T1D, a small subset undergoes senescence, a stress response involving growth arrest, DNA damage response, and activation of a senescence-associated secretory phenotype (SASP). SASP in beta cells of the nonobese diabetic (NOD) mouse model of T1D and primary human islets is regulated at the level of transcription by bromodomain extra-terminal (BET) proteins, but the mechanisms remain unclear. To explore how SASP is transcriptionally regulated in beta cells, we used the NOD beta cell line NIT-1 to model beta cell SASP and identified binding partners of BET protein Brd4 and explored the role of the cyclin-dependent kinase inhibitor p21. Brd4 interacted with a variety of proteins in senescent NIT-1 cells including subunits of the Ino80 chromatin remodeling complex, which was expressed in beta cells during T1D progression in NOD mice and in human beta cells of control, autoantibody-positive, and T1D donors as determined from single-cell RNA-seq data. RNAi knockdown of p21 during senescence in NIT-1 cells did not significantly impact viability or SASP. Taken together, these results suggest that Brd4 interacts with several protein partners during senescence in NIT-1 cells, some of which may play roles in SASP gene activation and that p21 is dispensable for the SASP in this beta cell model. Full article
Show Figures

Figure 1

2021

Jump to: 2024

14 pages, 9801 KiB  
Review
The Placenta as a Target of Epigenetic Alterations in Women with Gestational Diabetes Mellitus and Potential Implications for the Offspring
by Dennise Lizárraga and Alejandra García-Gasca
Epigenomes 2021, 5(2), 13; https://doi.org/10.3390/epigenomes5020013 - 10 May 2021
Cited by 11 | Viewed by 9289
Abstract
Gestational diabetes mellitus (GDM) is a pregnancy complication first detected in the second or third trimester in women that did not show evident glucose intolerance or diabetes before gestation. In 2019, the International Diabetes Federation reported that 15.8% of live births were affected [...] Read more.
Gestational diabetes mellitus (GDM) is a pregnancy complication first detected in the second or third trimester in women that did not show evident glucose intolerance or diabetes before gestation. In 2019, the International Diabetes Federation reported that 15.8% of live births were affected by hyperglycemia during pregnancy, of which 83.6% were due to gestational diabetes mellitus, 8.5% were due to diabetes first detected in pregnancy, and 7.9% were due to diabetes detected before pregnancy. GDM increases the susceptibility to developing chronic diseases for both the mother and the baby later in life. Under GDM conditions, the intrauterine environment becomes hyperglycemic, while also showing high concentrations of fatty acids and proinflammatory cytokines, producing morphological, structural, and molecular modifications in the placenta, affecting its function; these alterations may predispose the baby to disease in adult life. Molecular alterations include epigenetic mechanisms such as DNA and RNA methylation, chromatin remodeling, histone modifications, and expression of noncoding RNAs (ncRNAs). The placenta is a unique organ that originates only in pregnancy, and its main function is communication between the mother and the fetus, ensuring healthy development. Thus, this review provides up-to-date information regarding two of the best-documented (epigenetic) mechanisms (DNA methylation and miRNA expression) altered in the human placenta under GDM conditions, as well as potential implications for the offspring. Full article
Show Figures

Figure 1

Back to TopTop