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Cells
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Non-coding RNAs and Neurological Diseases 2022
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Non-coding RNAs and Neurological Diseases 2022

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 11002

Special Issue Editor

Prof. Dr. P. Hemachandra Reddy

E-Mail Website
Guest Editor
Department of Internal Medicine, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430-6540, USA
Interests: aging; mitochondrial dynamics; oxidative stress; mitophagy; neurodegeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The purpose of this Special Issue on “Non-Coding RNAs and Neurological Diseases 2022” is to discuss the recent developments in microRNAs and non-coding RNAs in neurological diseases. MicroRNAs are a large family of conserved, small (20–22 nucleotides in length), non-coding RNAs. miRNAs play a central role in the post-translational regulation of gene expression, and have been found to be important regulators of many diseases, including diabetes, stroke, cancer, and neurological diseases, such as stroke, Alzheimer’s, Parkinson’s, Huntington’s, multiple sclerosis, amyotrophic lateral sclerosis, and triple-repeat diseases. In mammals, miRNAs are reported to control about 50% of all protein-coding genes. Currently, over 2000 miRNAs have been identified (for details, see www.mirbase.org). One-third of these miRNAs are found in the coding part of genes, and the remaining are in the intronic regions. miRNAs are important regulators of several biological processes, such as cell growth, apoptosis, cell proliferation, embryonic development, and tissue differentiation. Long non-coding RNAs (LncRNAs) are a large and diverse class of non-coding RNAs, with a length of more than 200 nucleotides that do not encode proteins. LncRNAs are largely classified into different subtypes based on the position and direction of transcription in relation to other genes. LncRNAs are dynamic and have a wide range of roles in cellular and developmental processes, and in regulating gene expression. They are also useful in understanding the complexity of genomic regulation. The articles from this Special Issue will provide new information and critically assess the current status of microRNAs and long non-coding microRNAs in neurological diseases. A major focus of this Special Issue will be microRNAs and long non-coding RNAs as therapeutic targets and peripheral biomarkers in neurological diseases.

Prof. Dr. P. Hemachandra Reddy
Guest 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 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. Cells 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 2700 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.

Keywords

  • microRNAs
  • long non-coding RNAs
  • gene regulation
  • stroke
  • Alzheimer’s
  • Parkinson’s
  • Huntington’s
  • multiple sclerosis
  • amyotrophic lateral sclerosis
  • triple-repeat diseases

Published Papers (5 papers)

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Research

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20 pages, 4640 KiB  
Article
lncRNA Sequencing Reveals Neurodegeneration-Associated FUS Mutations Alter Transcriptional Landscape of iPS Cells That Persists in Motor Neurons
by Vincent E. Provasek, Manohar Kodavati, Wenting Guo, Haibo Wang, Istvan Boldogh, Ludo Van Den Bosch, Gavin Britz and Muralidhar L. Hegde
Cells 2023, 12(20), 2461; https://doi.org/10.3390/cells12202461 - 16 Oct 2023
Cited by 1 | Viewed by 1342
Abstract
Fused-in sarcoma (FUS) gene mutations have been implicated in amyotrophic lateral sclerosis (ALS). This study aimed to investigate the impact of FUS mutations (R521H and P525L) on the transcriptome of induced pluripotent stem cells (iPSCs) and iPSC-derived motor neurons (iMNs). Using RNA sequencing [...] Read more.
Fused-in sarcoma (FUS) gene mutations have been implicated in amyotrophic lateral sclerosis (ALS). This study aimed to investigate the impact of FUS mutations (R521H and P525L) on the transcriptome of induced pluripotent stem cells (iPSCs) and iPSC-derived motor neurons (iMNs). Using RNA sequencing (RNA Seq), we characterized differentially expressed genes (DEGs) and differentially expressed lncRNAs (DELs) and subsequently predicted lncRNA–mRNA target pairs (TAR pairs). Our results show that FUS mutations significantly altered the expression profiles of mRNAs and lncRNAs in iPSCs. Using this large dataset, we identified and verified six key differentially regulated TAR pairs in iPSCs that were also altered in iMNs. These target transcripts included: GPR149, NR4A, LMO3, SLC15A4, ZNF404, and CRACD. These findings indicated that selected mutant FUS-induced transcriptional alterations persist from iPSCs into differentiated iMNs. Functional enrichment analyses of DEGs indicated pathways associated with neuronal development and carcinogenesis as likely altered by these FUS mutations. Furthermore, ingenuity pathway analysis (IPA) and GO network analysis of lncRNA-targeted mRNAs indicated associations between RNA metabolism, lncRNA regulation, and DNA damage repair. Our findings provide insights into potential molecular mechanisms underlying the pathophysiology of ALS-associated FUS mutations and suggest potential therapeutic targets for the treatment of ALS. Full article
(This article belongs to the Special Issue Non-coding RNAs and Neurological Diseases 2022)
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18 pages, 3264 KiB  
Article
Functional Characterisation of the Circular RNA, circHTT(2-6), in Huntington’s Disease
by Laura Gantley, Brett W. Stringer, Vanessa M. Conn, Youichirou Ootsuka, Duncan Holds, Mark Slee, Kamelya Aliakbari, Kirsty Kirk, Rebecca J. Ormsby, Stuart T. Webb, Adrienne Hanson, He Lin, Luke A. Selth and Simon J. Conn
Cells 2023, 12(9), 1337; https://doi.org/10.3390/cells12091337 - 07 May 2023
Cited by 2 | Viewed by 2166
Abstract
Trinucleotide repeat disorders comprise ~20 severe, inherited, human neuromuscular and neurodegenerative disorders, which result from an abnormal expansion of repetitive sequences in the DNA. The most common of these, Huntington’s disease (HD), results from expansion of the CAG repeat region in exon 1 [...] Read more.
Trinucleotide repeat disorders comprise ~20 severe, inherited, human neuromuscular and neurodegenerative disorders, which result from an abnormal expansion of repetitive sequences in the DNA. The most common of these, Huntington’s disease (HD), results from expansion of the CAG repeat region in exon 1 of the HTT gene via an unknown mechanism. Since non-coding RNAs have been implicated in the initiation and progression of many diseases, herein we focused on a circular RNA (circRNA) molecule arising from non-canonical splicing (backsplicing) of HTT pre-mRNA. The most abundant circRNA from HTT, circHTT(2-6), was found to be more highly expressed in the frontal cortex of HD patients, compared with healthy controls, and positively correlated with CAG repeat tract length. Furthermore, the mouse orthologue (mmu_circHTT(2-6)) was found to be enriched within the brain and specifically the striatum, a region enriched for medium spiny neurons that are preferentially lost in HD. Transgenic overexpression of circHTT(2-6) in two human cell lines—SH-SY5Y and HEK293—reduced cell proliferation and nuclear size without affecting cell cycle progression or cellular size, or altering the CAG repeat region length within HTT. CircHTT(2-6) overexpression did not alter total HTT protein levels, but reduced its nuclear localisation. As these phenotypic and genotypic changes resemble those observed in HD patients, our results suggest that circHTT(2-6) may play a functional role in the pathophysiology of this disease. Full article
(This article belongs to the Special Issue Non-coding RNAs and Neurological Diseases 2022)
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19 pages, 3715 KiB  
Article
Characterizing Relevant MicroRNA Editing Sites in Parkinson’s Disease
by Chenyu Lu, Shuchao Ren, Wenping Xie, Zhigang Zhao, Xingwang Wu, Shiyong Guo, Angbaji Suo, Nan Zhou, Jun Yang, Shuai Wu and Yun Zheng
Cells 2023, 12(1), 75; https://doi.org/10.3390/cells12010075 - 24 Dec 2022
Cited by 3 | Viewed by 1218
Abstract
MicroRNAs (miRNAs) are extensively edited in human brains. However, the functional relevance of the miRNA editome is largely unknown in Parkinson’s disease (PD). By analyzing small RNA sequencing profiles of brain tissues of 43 PD patients and 88 normal controls, we found that [...] Read more.
MicroRNAs (miRNAs) are extensively edited in human brains. However, the functional relevance of the miRNA editome is largely unknown in Parkinson’s disease (PD). By analyzing small RNA sequencing profiles of brain tissues of 43 PD patients and 88 normal controls, we found that the editing levels of five A-to-I and two C-to-U editing sites are significantly correlated with the ages of normal controls, which is disrupted in PD patients. We totally identified 362 miRNA editing sites with significantly different editing levels in prefrontal cortices of PD patients (PD-PC) compared to results of normal controls. We experimentally validated that A-to-I edited miR-497-5p, with significantly higher expression levels in PD-PC compared to normal controls, directly represses OPA1 and VAPB. Furthermore, overexpression of A-to-I edited miR-497-5p downregulates OPA1 and VAPB in two cell lines, and inhibits proliferation of glioma cells. These results suggest that the hyperediting of miR-497-5p in PD contributes to enhanced progressive neurodegeneration of PD patients. Our results provide new insights into the mechanistic understanding, novel diagnostics, and therapeutic clues of PD. Full article
(This article belongs to the Special Issue Non-coding RNAs and Neurological Diseases 2022)
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Review

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19 pages, 6671 KiB  
Review
Emerging Roles of miRNA, lncRNA, circRNA, and Their Cross-Talk in Pituitary Adenoma
by Wentao Wu, Lei Cao, Yanfei Jia, Youchao Xiao, Xu Zhang and Songbai Gui
Cells 2022, 11(18), 2920; https://doi.org/10.3390/cells11182920 - 19 Sep 2022
Cited by 6 | Viewed by 2678
Abstract
Pituitary adenoma (PA) is a common intracranial tumor without specific biomarkers for diagnosis and treatment. Non-coding RNAs (ncRNAs), including microRNAs (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA), regulate a variety of cellular processes, such as cell proliferation, differentiation, and apoptosis. Increasing [...] Read more.
Pituitary adenoma (PA) is a common intracranial tumor without specific biomarkers for diagnosis and treatment. Non-coding RNAs (ncRNAs), including microRNAs (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA), regulate a variety of cellular processes, such as cell proliferation, differentiation, and apoptosis. Increasing studies have shown that the dysregulation of ncRNAs, especially the cross-talk between lncRNA/circRNA and miRNA, is related to the pathogenesis, diagnosis, and prognosis of PA. Therefore, ncRNAs can be considered as promising biomarkers for PA. In this review, we summarize the roles of ncRNAs from different specimens (i.e., tissues, biofluids, cells, and exosomes) in multiple subtypes of PA and highlight important advances in understanding the contribution of the cross-talk between ncRNAs (e.g., competing endogenous RNAs) to PA disease. Full article
(This article belongs to the Special Issue Non-coding RNAs and Neurological Diseases 2022)
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Other

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10 pages, 270 KiB  
Perspective
Mitochondria Localized microRNAs: An Unexplored miRNA Niche in Alzheimer’s Disease and Aging
by Jazmin Rivera, Laxman Gangwani and Subodh Kumar
Cells 2023, 12(5), 742; https://doi.org/10.3390/cells12050742 - 25 Feb 2023
Cited by 8 | Viewed by 2776
Abstract
Mitochondria play several vital roles in the brain cells, especially in neurons to provide synaptic energy (ATP), Ca2+ homeostasis, Reactive Oxygen Species (ROS) production, apoptosis, mitophagy, axonal transport and neurotransmission. Mitochondrial dysfunction is a well-established phenomenon in the pathophysiology of many neurological [...] Read more.
Mitochondria play several vital roles in the brain cells, especially in neurons to provide synaptic energy (ATP), Ca2+ homeostasis, Reactive Oxygen Species (ROS) production, apoptosis, mitophagy, axonal transport and neurotransmission. Mitochondrial dysfunction is a well-established phenomenon in the pathophysiology of many neurological diseases, including Alzheimer’s disease (AD). Amyloid-beta (Aβ) and Phosphorylated tau (p-tau) proteins cause the severe mitochondrial defects in AD. A newly discovered cellular niche of microRNAs (miRNAs), so-called mitochondrial-miRNAs (mito-miRs), has recently been explored in mitochondrial functions, cellular processes and in a few human diseases. The mitochondria localized miRNAs regulate local mitochondrial genes expression and are significantly involved in the modulation of mitochondrial proteins, and thereby in controlling mitochondrial function. Thus, mitochondrial miRNAs are crucial to maintaining mitochondrial integrity and for normal mitochondrial homeostasis. Mitochondrial dysfunction is well established in AD pathogenesis, but unfortunately mitochondria miRNAs and their precise roles have not yet been investigated in AD. Therefore, an urgent need exists to examine and decipher the critical roles of mitochondrial miRNAs in AD and in the aging process. The current perspective sheds light on the latest insights and future research directions on investigating the contribution of mitochondrial miRNAs in AD and aging. Full article
(This article belongs to the Special Issue Non-coding RNAs and Neurological Diseases 2022)
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