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miRNA-Mediated Post-transcriptional Regulation in the Nervous System
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miRNA-Mediated Post-transcriptional Regulation in the Nervous System

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 December 2023) | Viewed by 9467

Special Issue Editors

Dr. Cecilia Mannironi

E-Mail Website
Guest Editor
Institute of Molecular Biology and Pathology, National Research Council, 00185 Rome, Italy
Interests: post-transcriptional regulation; gene expression; nervous system; microRNA; ncRNA; circRNA
Dr. Francesca De Vito

E-Mail Website
Guest Editor
Neurology Unit, IRCSS Neuromed, 86077 Pozzilli, Italy
Interests: microRNAs; post-transcriptional; neuroimmunology; synaptic plasticity; multiple sclerosis; nutrition

Special Issue Information

Dear Colleagues,

MicroRNAs (miRNAs) are small noncoding RNAs (ncRNAs) that suppress the translation and/or initiate the degradation of target mRNAs. Each miRNA post-transcriptionally controls the expression of hundreds of genes, modulating signaling cascades and entire pathways. In the central nervous system (CNS), miRNAs have diverse and highly specific spatio-temporal patterns of expression and function. Two decades of functional and molecular studies on neuronal miRNAs have clearly demonstrated that they are key regulators of neuronal differentiation, brain development and plasticity mechanisms in post-natal neurons. Interestingly, external stimuli and neuronal activity modulate their expression and function, through regulatory pathways that involve RNA binding proteins (RPBs) and other RNA interactors. The essential contribution of miRNAs to brain homeostasis is proven by the fact that miRNA loss of function or dysregulation is highly associated with neuronal diseases. Indeed, recent pieces of evidence have indicated the role of many miRNAs in the etiology of human neurodevelopmental and neurodegenerative diseases.

This Special Issue aims to discuss recent findings on the molecular mechanism of miRNA-dependent gene expression regulation in the CNS. A special focus will be on newly discovered molecular networks involving miRNAs, other ncRNAs or RBPs, acting in brain physiology and pathology. We welcome original research, reviews and other article types.

Dr. Cecilia Mannironi
Dr. Francesca De Vito
Guest Editors

Manuscript Submission Information

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Keywords

  • neuronal miRNA
  • miRNA biogenesis
  • miRNA activity
  • RNA stability
  • circRNA
  • lncRNA
  • RNA binding proteins
  • extracellular macrovesicle
  • synaptic transmission
  • CNS pathology

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Published Papers (4 papers)

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Research

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15 pages, 2301 KiB  
Article
Interaction between miR-142-3p and BDNF Val/Met Polymorphism Regulates Multiple Sclerosis Severity
by Ettore Dolcetti, Alessandra Musella, Sara Balletta, Luana Gilio, Antonio Bruno, Mario Stampanoni Bassi, Gianluca Lauritano, Fabio Buttari, Diego Fresegna, Alice Tartacca, Fabrizio Mariani, Federica Palmerio, Valentina Rovella, Rosangela Ferese, Stefano Gambardella, Emiliano Giardina, Annamaria Finardi, Roberto Furlan, Georgia Mandolesi, Diego Centonze and Francesca De Vitoadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2024, 25(10), 5253; https://doi.org/10.3390/ijms25105253 - 11 May 2024
Viewed by 1031
Abstract
MiR-142-3p has recently emerged as key factor in tailoring personalized treatments for multiple sclerosis (MS), a chronic autoimmune demyelinating disease of the central nervous system (CNS) with heterogeneous pathophysiology and an unpredictable course. With its involvement in a detrimental regulatory axis with interleukin-1beta [...] Read more.
MiR-142-3p has recently emerged as key factor in tailoring personalized treatments for multiple sclerosis (MS), a chronic autoimmune demyelinating disease of the central nervous system (CNS) with heterogeneous pathophysiology and an unpredictable course. With its involvement in a detrimental regulatory axis with interleukin-1beta (IL1β), miR-142-3p orchestrates excitotoxic synaptic alterations that significantly impact both MS progression and therapeutic outcomes. In this study, we investigated for the first time the influence of individual genetic variability on the miR-142-3p excitotoxic effect in MS. We specifically focused on the single-nucleotide polymorphism Val66Met (rs6265) of the brain-derived neurotrophic factor (BDNF) gene, known for its crucial role in CNS functioning. We assessed the levels of miR-142-3p and IL1β in cerebrospinal fluid (CSF) obtained from a cohort of 114 patients with MS upon diagnosis. By stratifying patients according to their genetic background, statistical correlations with clinical parameters were performed. Notably, in Met-carrier patients, we observed a decoupling of miR-142-3p levels from IL1β levels in the CSF, as well as from of disease severity (Expanded Disability Status Score, EDSS; Multiple Sclerosis Severity Score, MSSS; Age-Related Multiple Sclerosis Severity Score, ARMSS) and progression (Progression Index, PI). Our discovery of the interference between BDNF Val66Met polymorphism and the synaptotoxic IL1β-miR-142-3p axis, therefore hampering miR-142-3p action on MS course, provides valuable insights for further development of personalized medicine in the field. Full article
(This article belongs to the Special Issue miRNA-Mediated Post-transcriptional Regulation in the Nervous System)
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25 pages, 3473 KiB  
Article
Oral Delivery of miR-320-3p with Lipidic Aminoglycoside Derivatives at Mid-Lactation Alters miR-320-3p Endogenous Levels in the Gut and Brain of Adult Rats According to Early or Regular Weaning
by Gabriel Araujo Tavares, Amada Torres, Gwenola Le Drean, Maïwenn Queignec, Blandine Castellano, Laurent Tesson, Séverine Remy, Ignacio Anegon, Bruno Pitard and Bertrand Kaeffer
Int. J. Mol. Sci. 2023, 24(1), 191; https://doi.org/10.3390/ijms24010191 - 22 Dec 2022
Cited by 2 | Viewed by 2486
Abstract
To investigate if the artificial delivery of microRNAs naturally present in the breastmilk can impact the gut and brain of young rats according to weaning. Animals from a new transgenic rat line expressing the green-fluorescent protein in the endocrine lineage (cholecystokinin expressing cells) [...] Read more.
To investigate if the artificial delivery of microRNAs naturally present in the breastmilk can impact the gut and brain of young rats according to weaning. Animals from a new transgenic rat line expressing the green-fluorescent protein in the endocrine lineage (cholecystokinin expressing cells) received a single oral bolus of miR-320-3p or miR-375-3p embedded in DiOleyl-Succinyl-Paromomycin (DOSP) on D-12. The pups were weaned early (D-15), or regularly (D-30). The expression of relevant miRNA, mRNAs, chromatin complexes, and duodenal cell density were assessed at 8 h post-inoculation and on D-45. The miR-320-3p/DOSP induced immediate effects on H3K4me3 chromatin complexes with polr3d promoter (p < 0.05). On regular weaning, on D-45, miR-320-3p and 375-3p were found to be downregulated in the stomach and upregulated in the hypothalamus (p < 0.001), whereas miR-320-3p was upregulated in the duodenum. After early weaning, miR-320-3p and miR-375-3p were downregulated in the stomach and the duodenum, but upregulated in the hypothalamus and the hippocampus. Combination of miR-320-3p/DOSP with early weaning enhanced miR-320-3p and chromogranin A expression in the duodenum. In the female brain stem, miR-320-3p, miR-504, and miR-16-5p levels were all upregulated. Investigating the oral miRNA-320-3p loads in the duodenal cell lineage paved the way for designing new therapeutics to avoid unexpected long-term impacts on the brain. Full article
(This article belongs to the Special Issue miRNA-Mediated Post-transcriptional Regulation in the Nervous System)
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Review

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19 pages, 1240 KiB  
Review
Sex-Biased Expression and Response of microRNAs in Neurological Diseases and Neurotrauma
by Urim Geleta, Paresh Prajapati, Adam Bachstetter, Peter T. Nelson and Wang-Xia Wang
Int. J. Mol. Sci. 2024, 25(5), 2648; https://doi.org/10.3390/ijms25052648 - 24 Feb 2024
Viewed by 1523
Abstract
Neurological diseases and neurotrauma manifest significant sex differences in prevalence, progression, outcome, and therapeutic responses. Genetic predisposition, sex hormones, inflammation, and environmental exposures are among many physiological and pathological factors that impact the sex disparity in neurological diseases. MicroRNAs (miRNAs) are a powerful [...] Read more.
Neurological diseases and neurotrauma manifest significant sex differences in prevalence, progression, outcome, and therapeutic responses. Genetic predisposition, sex hormones, inflammation, and environmental exposures are among many physiological and pathological factors that impact the sex disparity in neurological diseases. MicroRNAs (miRNAs) are a powerful class of gene expression regulator that are extensively involved in mediating biological pathways. Emerging evidence demonstrates that miRNAs play a crucial role in the sex dimorphism observed in various human diseases, including neurological diseases. Understanding the sex differences in miRNA expression and response is believed to have important implications for assessing the risk of neurological disease, defining therapeutic intervention strategies, and advancing both basic research and clinical investigations. However, there is limited research exploring the extent to which miRNAs contribute to the sex disparities observed in various neurological diseases. Here, we review the current state of knowledge related to the sexual dimorphism in miRNAs in neurological diseases and neurotrauma research. We also discuss how sex chromosomes may contribute to the miRNA sexual dimorphism phenomenon. We attempt to emphasize the significance of sexual dimorphism in miRNA biology in human diseases and to advocate a gender/sex-balanced science. Full article
(This article belongs to the Special Issue miRNA-Mediated Post-transcriptional Regulation in the Nervous System)
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19 pages, 1135 KiB  
Review
The Impact of Dysregulated microRNA Biogenesis Machinery and microRNA Sorting on Neurodegenerative Diseases
by Yu-Ting Weng, Yao-Ming Chang and Yijuang Chern
Int. J. Mol. Sci. 2023, 24(4), 3443; https://doi.org/10.3390/ijms24043443 - 8 Feb 2023
Cited by 9 | Viewed by 3559
Abstract
MicroRNAs (miRNAs) are 22-nucleotide noncoding RNAs involved in the differentiation, development, and function of cells in the body by targeting the 3′- untranslated regions (UTR) of mRNAs for degradation or translational inhibition. miRNAs not only affect gene expression inside the cells but also, [...] Read more.
MicroRNAs (miRNAs) are 22-nucleotide noncoding RNAs involved in the differentiation, development, and function of cells in the body by targeting the 3′- untranslated regions (UTR) of mRNAs for degradation or translational inhibition. miRNAs not only affect gene expression inside the cells but also, when sorted into exosomes, systemically mediate the communication between different types of cells. Neurodegenerative diseases (NDs) are age-associated, chronic neurological diseases characterized by the aggregation of misfolded proteins, which results in the progressive degeneration of selected neuronal population(s). The dysregulation of biogenesis and/or sorting of miRNAs into exosomes was reported in several NDs, including Huntington’s disease (HD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Alzheimer’s disease (AD). Many studies support the possible roles of dysregulated miRNAs in NDs as biomarkers and therapeutic treatments. Understanding the molecular mechanisms underlying the dysregulated miRNAs in NDs is therefore timely and important for the development of diagnostic and therapeutic interventions. In this review, we focus on the dysregulated miRNA machinery and the role of RNA-binding proteins (RBPs) in NDs. The tools that are available to identify the target miRNA-mRNA axes in NDs in an unbiased manner are also discussed. Full article
(This article belongs to the Special Issue miRNA-Mediated Post-transcriptional Regulation in the Nervous System)
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