Epigenetics and Cell-to-Cell Communication

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Epigenomics".

Deadline for manuscript submissions: closed (25 February 2023) | Viewed by 4493

Special Issue Editor


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Guest Editor
Department Biomedicine, Neurosciences and Advanced Diagnostics (Bi.N.D.), Universita degli Studi di Palermo, Palermo, Italy
Interests: brain cells; blood-brain barrier; RNA-binding proteins; extracellular vesicles; histone variants
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Special Issue Information

Dear Colleagues,

One of the most amazing properties of the cells of eukaryotic organisms is their ability to acquire very different phenotypes, both in development and in response to environmental cues, even if they all rely on the same genetic patrimony. This is possible because DNA is condensed with a number of proteins, thus forming a nucleoprotein complex known as chromatin. The post-translational modification of proteins, as well as DNA methylation, can regulate the overall structure of chromatin as well as the structural organization of specific genes, thus allowing differential gene expression in different cells. Notably, extracellular signals can induce modifications of chromatin arrangements. Most important, acquired chromatin structures and, consequently, cell phenotypes can be transmitted across cell generations.

In this context, cell-to-cell communications have a fundamental role. In particular, in the last few decades the role of extracellular vesicles (EVs) in transferring molecules (i.e., proteins, mRNAs, non-coding RNAs, and lipids) from almost all cell types to the surrounding ones has been recognized, thus inducing epigenetic modifications of gene expression in the receiving cells. The aim of this Special Issue is to analyze and discuss the role of these epigenetic events in physiological conditions as well as in pathologies such as cancer and neurodegeneration.

Prof. Dr. Italia Di Liegro
Guest Editor

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Keywords

  • chromatin structure and epigenetics
  • cell-to-cell communications
  • histone modifications
  • extracellular vesicles
  • post-transcriptional regulation
  • RNA-binding proteins

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Published Papers (2 papers)

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Research

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13 pages, 2456 KiB  
Article
An In Vitro Model of Glioma Development
by Gabriella Schiera, Patrizia Cancemi, Carlo Maria Di Liegro, Flores Naselli, Sara Volpes, Ilenia Cruciata, Paola Sofia Cardinale, Fabiola Vaglica, Matteo Calligaris, Anna Paola Carreca, Roberto Chiarelli, Simone Dario Scilabra, Olga Leone, Fabio Caradonna and Italia Di Liegro
Genes 2023, 14(5), 990; https://doi.org/10.3390/genes14050990 - 27 Apr 2023
Cited by 3 | Viewed by 1729
Abstract
Gliomas are the prevalent forms of brain cancer and derive from glial cells. Among them, astrocytomas are the most frequent. Astrocytes are fundamental for most brain functions, as they contribute to neuronal metabolism and neurotransmission. When they acquire cancer properties, their functions are [...] Read more.
Gliomas are the prevalent forms of brain cancer and derive from glial cells. Among them, astrocytomas are the most frequent. Astrocytes are fundamental for most brain functions, as they contribute to neuronal metabolism and neurotransmission. When they acquire cancer properties, their functions are altered, and, in addition, they start invading the brain parenchyma. Thus, a better knowledge of transformed astrocyte molecular properties is essential. With this aim, we previously developed rat astrocyte clones with increasing cancer properties. In this study, we used proteomic analysis to compare the most transformed clone (A-FC6) with normal primary astrocytes. We found that 154 proteins are downregulated and 101 upregulated in the clone. Moreover, 46 proteins are only expressed in the clone and 82 only in the normal cells. Notably, only 11 upregulated/unique proteins are encoded in the duplicated q arm of isochromosome 8 (i(8q)), which cytogenetically characterizes the clone. Since both normal and transformed brain cells release extracellular vesicles (EVs), which might induce epigenetic modifications in the neighboring cells, we also compared EVs released from transformed and normal astrocytes. Interestingly, we found that the clone releases EVs containing proteins, such as matrix metalloproteinase 3 (MMP3), that can modify the extracellular matrix, thus allowing invasion. Full article
(This article belongs to the Special Issue Epigenetics and Cell-to-Cell Communication)
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Review

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17 pages, 2280 KiB  
Review
Comparison on Major Gene Mutations Related to Rifampicin and Isoniazid Resistance between Beijing and Non-Beijing Strains of Mycobacterium tuberculosis: A Systematic Review and Bayesian Meta-Analysis
by Shengqiong Guo, Virasakdi Chongsuvivatwong and Shiguang Lei
Genes 2022, 13(10), 1849; https://doi.org/10.3390/genes13101849 - 13 Oct 2022
Cited by 1 | Viewed by 2250
Abstract
Objective: The Beijing strain of Mycobacterium tuberculosis (MTB) is controversially presented as the predominant genotype and is more drug resistant to rifampicin and isoniazid compared to the non-Beijing strain. We aimed to compare the major gene mutations related to rifampicin and isoniazid drug [...] Read more.
Objective: The Beijing strain of Mycobacterium tuberculosis (MTB) is controversially presented as the predominant genotype and is more drug resistant to rifampicin and isoniazid compared to the non-Beijing strain. We aimed to compare the major gene mutations related to rifampicin and isoniazid drug resistance between Beijing and non-Beijing genotypes, and to extract the best evidence using the evidence-based methods for improving the service of TB control programs based on genetics of MTB. Method: Literature was searched in Google Scholar, PubMed and CNKI Database. Data analysis was conducted in R software. The conventional and Bayesian random-effects models were employed for meta-analysis, combining the examinations of publication bias and sensitivity. Results: Of the 8785 strains in the pooled studies, 5225 were identified as Beijing strains and 3560 as non-Beijing strains. The maximum and minimum strain sizes were 876 and 55, respectively. The mutations prevalence of rpoB, katG, inhA and oxyR-ahpC in Beijing strains was 52.40% (2738/5225), 57.88% (2781/4805), 12.75% (454/3562) and 6.26% (108/1724), respectively, and that in non-Beijing strains was 26.12% (930/3560), 28.65% (834/2911), 10.67% (157/1472) and 7.21% (33/458), separately. The pooled posterior value of OR for the mutations of rpoB was 2.72 ((95% confidence interval (CI): 1.90, 3.94) times higher in Beijing than in non-Beijing strains. That value for katG was 3.22 (95% CI: 2.12, 4.90) times. The estimate for inhA was 1.41 (95% CI: 0.97, 2.08) times higher in the non-Beijing than in Beijing strains. That for oxyR-ahpC was 1.46 (95% CI: 0.87, 2.48) times. The principal patterns of the variants for the mutations of the four genes were rpoB S531L, katG S315T, inhA-15C > T and oxyR-ahpC intergenic region. Conclusion: The mutations in rpoB and katG genes in Beijing are significantly more common than that in non-Beijing strains of MTB. We do not have sufficient evidence to support that the prevalence of mutations of inhA and oxyR-ahpC is higher in non-Beijing than in Beijing strains, which provides a reference basis for clinical medication selection. Full article
(This article belongs to the Special Issue Epigenetics and Cell-to-Cell Communication)
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