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Cells
Special Issues
MicroRNA-Mediated Gene Regulation in Health and Disease
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MicroRNA-Mediated Gene Regulation in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (20 April 2023) | Viewed by 12753

Special Issue Editor

Dr. Neil Renwick

E-Mail Website
Guest Editor
Laboratory of Translational RNA Biology, Department of Pathology and Molecular Medicine, Queen’s University, 88 Stuart St, Kingston, ON K7L 3N6, Canada
Interests: rare cancer; microRNA; microRNA genetics; microRNA expression; microRNA targeting; microRNA dysregulation; disease mechanisms; disease models; microRNA diagnostics; microRNA therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

MicroRNAs (miRNAs) are small (19-24 nt) RNA molecules that negatively regulate gene expression. These molecules control many biological processes, including development, differentiation, cell proliferation, and apoptosis. They are also dysregulated in many diseases, often exhibiting disease-type and -stage expression patterns. Over the past two decades, it has become increasingly clear that miRNAs can provide valuable insights into biological and pathological processes through predictable messenger RNA targeting. In this Special Issue, we focus on clinical, biological, and computational studies of miRNAs and their targets in human cells and tissues. We are particularly interested in novel miRNA detection methods, cross-platform analyses of existing methods, miRNA and target sequence genetic variation, the miRNA expression profiling of biological and clinical samples, computational and/or experimental target identification, miRNA-based therapeutic approaches, and machine learning and other advanced computational approaches for classifying samples and/or studying miRNA-mRNA regulatory networks. A fuller understanding of miRNA-mediated gene regulation in health and disease will advance our knowledge of human cell biology and pave the way to identifying novel diagnostic and therapeutic approaches for many diseases. 

Dr. Neil Renwick
Guest Editor

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Published Papers (4 papers)

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Research

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16 pages, 1892 KiB  
Article
Systems Genomics Reveals microRNA Regulation of ICS Response in Childhood Asthma
by Rinku Sharma, Anshul Tiwari, Alvin T. Kho, Juan C. Celedón, Scott T. Weiss, Kelan G. Tantisira and Michael J. McGeachie
Cells 2023, 12(11), 1505; https://doi.org/10.3390/cells12111505 - 29 May 2023
Cited by 2 | Viewed by 2045
Abstract
Background: Asthmatic patients’ responses to inhaled corticosteroids (ICS) are variable and difficult to quantify. We have previously defined a Cross-sectional Asthma STEroid Response (CASTER) measure of ICS response. MicroRNAs (miRNAs) have shown strong effects on asthma and inflammatory processes. Objective: The purpose of [...] Read more.
Background: Asthmatic patients’ responses to inhaled corticosteroids (ICS) are variable and difficult to quantify. We have previously defined a Cross-sectional Asthma STEroid Response (CASTER) measure of ICS response. MicroRNAs (miRNAs) have shown strong effects on asthma and inflammatory processes. Objective: The purpose of this study was to identify key associations between circulating miRNAs and ICS response in childhood asthma. Methods: Small RNA sequencing in peripheral blood serum from 580 children with asthma on ICS treatment from The Genetics of Asthma in Costa Rica Study (GACRS) was used to identify miRNAs associated with ICS response using generalized linear models. Replication was conducted in children on ICS from the Childhood Asthma Management Program (CAMP) cohort. The association between replicated miRNAs and the transcriptome of lymphoblastoid cell lines in response to a glucocorticoid was assessed. Results: The association study on the GACRS cohort identified 36 miRNAs associated with ICS response at 10% false discovery rate (FDR), three of which (miR-28-5p, miR-339-3p, and miR-432-5p) were in the same direction of effect and significant in the CAMP replication cohort. In addition, in vitro steroid response lymphoblastoid gene expression analysis revealed 22 dexamethasone responsive genes were significantly associated with three replicated miRNAs. Furthermore, Weighted Gene Co-expression Network Analysis (WGCNA) revealed a significant association between miR-339-3p and two modules (black and magenta) of genes associated with immune response and inflammation pathways. Conclusion: This study highlighted significant association between circulating miRNAs miR-28-5p, miR-339-3p, and miR-432-5p and ICS response. miR-339-3p may be involved in immune dysregulation, which leads to a poor response to ICS treatment. Full article
(This article belongs to the Special Issue MicroRNA-Mediated Gene Regulation in Health and Disease)
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15 pages, 2944 KiB  
Article
Induction of miR-665-3p Impairs the Differentiation of Myogenic Progenitor Cells by Regulating the TWF1-YAP1 Axis
by Mai Thi Nguyen and Wan Lee
Cells 2023, 12(8), 1114; https://doi.org/10.3390/cells12081114 - 8 Apr 2023
Viewed by 1562
Abstract
Actin dynamics are known to orchestrate various myogenic processes in progenitor cells. Twinfilin-1 (TWF1) is an actin-depolymerizing factor that plays a crucial role in the differentiation of myogenic progenitor cells. However, little is known about the mechanisms underlying the epigenetic regulation of TWF1 [...] Read more.
Actin dynamics are known to orchestrate various myogenic processes in progenitor cells. Twinfilin-1 (TWF1) is an actin-depolymerizing factor that plays a crucial role in the differentiation of myogenic progenitor cells. However, little is known about the mechanisms underlying the epigenetic regulation of TWF1 expression and impaired myogenic differentiation in the background of muscle wasting. This study investigated how miR-665-3p affects TWF1 expression, actin filaments’ modulation, proliferation, and myogenic differentiation in progenitor cells. Palmitic acid, the most prevalent saturated fatty acid (SFA) in food, suppressed TWF1 expression and inhibited the myogenic differentiation of C2C12 cells while increasing the level of miR-665-3p expression. Interestingly, miR-665-3p inhibited TWF1 expression by targeting TWF1 3′UTR directly. In addition, miR-665-3p accumulated filamentous actin (F-actin) and enhanced the nuclear translocation of Yes-associated protein 1 (YAP1), consequently promoting cell cycle progression and proliferation. Furthermore, miR-665-3p suppressed the expressions of myogenic factors, i.e., MyoD, MyoG, and MyHC, and consequently impaired myoblast differentiation. In conclusion, this study suggests that SFA-inducible miR-665-3p suppresses TWF1 expression epigenetically and inhibits myogenic differentiation by facilitating myoblast proliferation via the F-actin/YAP1 axis. Full article
(This article belongs to the Special Issue MicroRNA-Mediated Gene Regulation in Health and Disease)
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Review

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13 pages, 1486 KiB  
Review
Network Regulation of microRNA Biogenesis and Target Interaction
by Shintaro Komatsu, Hiroki Kitai and Hiroshi I. Suzuki
Cells 2023, 12(2), 306; https://doi.org/10.3390/cells12020306 - 13 Jan 2023
Cited by 44 | Viewed by 5437
Abstract
MicroRNAs (miRNAs) are versatile, post-transcriptional regulators of gene expression. Canonical miRNAs are generated through the two-step DROSHA- and DICER-mediated processing of primary miRNA (pri-miRNA) transcripts with optimal or suboptimal features for DROSHA and DICER cleavage and loading into Argonaute (AGO) proteins, whereas multiple [...] Read more.
MicroRNAs (miRNAs) are versatile, post-transcriptional regulators of gene expression. Canonical miRNAs are generated through the two-step DROSHA- and DICER-mediated processing of primary miRNA (pri-miRNA) transcripts with optimal or suboptimal features for DROSHA and DICER cleavage and loading into Argonaute (AGO) proteins, whereas multiple hairpin-structured RNAs are encoded in the genome and could be a source of non-canonical miRNAs. Recent advances in miRNA biogenesis research have revealed details of the structural basis of miRNA processing and cluster assistance mechanisms that facilitate the processing of suboptimal hairpins encoded together with optimal hairpins in polycistronic pri-miRNAs. In addition, a deeper investigation of miRNA–target interaction has provided insights into the complexity of target recognition with distinct outcomes, including target-mediated miRNA degradation (TDMD) and cooperation in target regulation by multiple miRNAs. Therefore, the coordinated or network regulation of both miRNA biogenesis and miRNA–target interaction is prevalent in miRNA biology. Alongside recent advances in the mechanistic investigation of miRNA functions, this review summarizes recent findings regarding the ordered regulation of miRNA biogenesis and miRNA–target interaction. Full article
(This article belongs to the Special Issue MicroRNA-Mediated Gene Regulation in Health and Disease)
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17 pages, 2029 KiB  
Review
The Complex Interaction between P53 and miRNAs Joins New Awareness in Physiological Stress Responses
by Camilla Capaccia, Silvana Diverio, Danilo Zampini and Gabriella Guelfi
Cells 2022, 11(10), 1631; https://doi.org/10.3390/cells11101631 - 13 May 2022
Cited by 9 | Viewed by 2711
Abstract
This review emphasizes the important role of cross-talk between P53 and microRNAs in physiological stress signaling. P53 responds to stress in a variety of ways ranging from activating survival-promotion pathways to triggering programmed cell death to eliminate damaged cells. In physiological stress generated [...] Read more.
This review emphasizes the important role of cross-talk between P53 and microRNAs in physiological stress signaling. P53 responds to stress in a variety of ways ranging from activating survival-promotion pathways to triggering programmed cell death to eliminate damaged cells. In physiological stress generated by any external or internal condition that challenges cell homeostasis, P53 exerts its function as a transcription factor for target genes or by regulating the expression and maturation of a class of small non-coding RNA molecules (miRNAs). The miRNAs control the level of P53 through direct control of P53 or through indirect control of P53 by targeting its regulators (such as MDMs). In turn, P53 controls the expression level of miRNAs targeted by P53 through the regulation of their transcription or biogenesis. This elaborate regulatory scheme emphasizes the relevance of miRNAs in the P53 network and vice versa. Full article
(This article belongs to the Special Issue MicroRNA-Mediated Gene Regulation in Health and Disease)
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