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Статті в журналах з теми "RNA pathogenesis"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Chatterjee, Biswanath, Che-Kun James Shen, and Pritha Majumder. "RNA Modifications and RNA Metabolism in Neurological Disease Pathogenesis." International Journal of Molecular Sciences 22, no. 21 (November 1, 2021): 11870. http://dx.doi.org/10.3390/ijms222111870.

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Анотація:

The intrinsic cellular heterogeneity and molecular complexity of the mammalian nervous system relies substantially on the dynamic nature and spatiotemporal patterning of gene expression. These features of gene expression are achieved in part through mechanisms involving various epigenetic processes such as DNA methylation, post-translational histone modifications, and non-coding RNA activity, amongst others. In concert, another regulatory layer by which RNA bases and sugar residues are chemically modified enhances neuronal transcriptome complexity. Similar RNA modifications in other systems collectively constitute the cellular epitranscriptome that integrates and impacts various physiological processes. The epitranscriptome is dynamic and is reshaped constantly to regulate vital processes such as development, differentiation and stress responses. Perturbations of the epitranscriptome can lead to various pathogenic conditions, including cancer, cardiovascular abnormalities and neurological diseases. Recent advances in next-generation sequencing technologies have enabled us to identify and locate modified bases/sugars on different RNA species. These RNA modifications modulate the stability, transport and, most importantly, translation of RNA. In this review, we discuss the formation and functions of some frequently observed RNA modifications—including methylations of adenine and cytosine bases, and isomerization of uridine to pseudouridine—at various layers of RNA metabolism, together with their contributions to abnormal physiological conditions that can lead to various neurodevelopmental and neurological disorders.

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2

Karst, Stephanie M. "Pathogenesis of Noroviruses, Emerging RNA Viruses." Viruses 2, no. 3 (March 23, 2010): 748–81. http://dx.doi.org/10.3390/v2030748.

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3

Baysal, Bora E., Shraddha Sharma, Seyedsasan Hashemikhabir, and Sarath Chandra Janga. "RNA Editing in Pathogenesis of Cancer." Cancer Research 77, no. 14 (June 30, 2017): 3733–39. http://dx.doi.org/10.1158/0008-5472.can-17-0520.

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4

Day, John W., and Laura P. W. Ranum. "RNA pathogenesis of the myotonic dystrophies." Neuromuscular Disorders 15, no. 1 (January 2005): 5–16. http://dx.doi.org/10.1016/j.nmd.2004.09.012.

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5

Pekarsky, Yuri, and Carlo M. Croce. "Noncoding RNA genes in cancer pathogenesis." Advances in Biological Regulation 71 (January 2019): 219–23. http://dx.doi.org/10.1016/j.jbior.2018.12.002.

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6

Poltronieri, Palmiro, Binlian Sun, and Massimo Mallardo. "RNA Viruses: RNA Roles in Pathogenesis, Coreplication and Viral Load." Current Genomics 16, no. 5 (July 10, 2015): 327–35. http://dx.doi.org/10.2174/1389202916666150707160613.

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7

Romano, Giulia, Michela Saviana, Patricia Le, Howard Li, Lavender Micalo, Giovanni Nigita, Mario Acunzo, and Patrick Nana-Sinkam. "Non-Coding RNA Editing in Cancer Pathogenesis." Cancers 12, no. 7 (July 8, 2020): 1845. http://dx.doi.org/10.3390/cancers12071845.

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Анотація:

In the last two decades, RNA post-transcriptional modifications, including RNA editing, have been the subject of increasing interest among the scientific community. The efforts of the Human Genome Project combined with the development of new sequencing technologies and dedicated bioinformatic approaches created to detect and profile RNA transcripts have served to further our understanding of RNA editing. Investigators have determined that non-coding RNA (ncRNA) A-to-I editing is often deregulated in cancer. This discovery has led to an increased number of published studies in the field. However, the eventual clinical application for these findings remains a work in progress. In this review, we provide an overview of the ncRNA editing phenomenon in cancer. We discuss the bioinformatic strategies for RNA editing detection as well as the potential roles for ncRNA A to I editing in tumor immunity and as clinical biomarkers.

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8

Gipson, Theresa A., Andreas Neueder, Nancy S. Wexler, Gillian P. Bates, and David Housman. "Aberrantly splicedHTT,a new player in Huntington’s disease pathogenesis." RNA Biology 10, no. 11 (November 2013): 1647–52. http://dx.doi.org/10.4161/rna.26706.

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9

Ranum, Laura P. W., and John W. Day. "Myotonic Dystrophy: RNA Pathogenesis Comes into Focus." American Journal of Human Genetics 74, no. 5 (May 2004): 793–804. http://dx.doi.org/10.1086/383590.

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10

Hu, Wen-Yuan, Christopher P. Myers, Jennifer M. Kilzer, Samuel L. Pfaff, and Frederic D. Bushman. "Inhibition of Retroviral Pathogenesis by RNA Interference." Current Biology 12, no. 15 (August 2002): 1301–11. http://dx.doi.org/10.1016/s0960-9822(02)00975-2.

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11

Arnvig, Kristine, and Douglas Young. "Non-coding RNA and its potential role in Mycobacterium tuberculosis pathogenesis." RNA Biology 9, no. 4 (April 2012): 427–36. http://dx.doi.org/10.4161/rna.20105.

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12

FIGUEROA, BRYAN E., and ROBERT M. FRIEDLANDER. "“Leaching RNA”: A New Model of Disease Pathogenesis." Neurosurgery 54, no. 5 (May 2004): N7. http://dx.doi.org/10.1227/01.neu.0000309629.77982.c3.

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13

Trobaugh, Derek W., and William B. Klimstra. "MicroRNA Regulation of RNA Virus Replication and Pathogenesis." Trends in Molecular Medicine 23, no. 1 (January 2017): 80–93. http://dx.doi.org/10.1016/j.molmed.2016.11.003.

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14

Tan, Huiping, He Li, and Peng Jin. "RNA-mediated pathogenesis in fragile X-associated disorders." Neuroscience Letters 466, no. 2 (December 2009): 103–8. http://dx.doi.org/10.1016/j.neulet.2009.07.053.

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15

Obeng, Esther A., Connor Stewart, and Omar Abdel-Wahab. "Altered RNA Processing in Cancer Pathogenesis and Therapy." Cancer Discovery 9, no. 11 (October 14, 2019): 1493–510. http://dx.doi.org/10.1158/2159-8290.cd-19-0399.

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16

Lu, Bingwei, Stephan Gehrke, and Zhihao Wu. "RNA metabolism in the pathogenesis of Parkinson׳s disease." Brain Research 1584 (October 2014): 105–15. http://dx.doi.org/10.1016/j.brainres.2014.03.003.

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17

Li, Yun R., Oliver D. King, James Shorter, and Aaron D. Gitler. "Stress granules as crucibles of ALS pathogenesis." Journal of Cell Biology 201, no. 3 (April 29, 2013): 361–72. http://dx.doi.org/10.1083/jcb.201302044.

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Анотація:

Amyotrophic lateral sclerosis (ALS) is a fatal human neurodegenerative disease affecting primarily motor neurons. Two RNA-binding proteins, TDP-43 and FUS, aggregate in the degenerating motor neurons of ALS patients, and mutations in the genes encoding these proteins cause some forms of ALS. TDP-43 and FUS and several related RNA-binding proteins harbor aggregation-promoting prion-like domains that allow them to rapidly self-associate. This property is critical for the formation and dynamics of cellular ribonucleoprotein granules, the crucibles of RNA metabolism and homeostasis. Recent work connecting TDP-43 and FUS to stress granules has suggested how this cellular pathway, which involves protein aggregation as part of its normal function, might be coopted during disease pathogenesis.

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18

Du, Shujuan, Xiaoqing Liu, and Qiliang Cai. "Viral-Mediated mRNA Degradation for Pathogenesis." Biomedicines 6, no. 4 (November 29, 2018): 111. http://dx.doi.org/10.3390/biomedicines6040111.

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Cellular RNA decay machinery plays a vital role in regulating gene expression by altering the stability of mRNAs in response to external stresses, including viral infection. In the primary infection, viruses often conquer the host cell’s antiviral immune response by controlling the inherently cellular mRNA degradation machinery to facilitate viral gene expression and establish a successful infection. This review summarizes the current knowledge about the diverse strategies of viral-mediated regulatory RNA shutoff for pathogenesis, and particularly sheds a light on the mechanisms that viruses evolve to elude immune surveillance during infection.

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19

Mallik, Moushami, та Subhash C. Lakhotia. "RNAi for the large non-coding hsrω transcripts suppresses polyglutamine pathogenesis inDrosophilamodels". RNA Biology 6, № 4 (вересень 2009): 464–78. http://dx.doi.org/10.4161/rna.6.4.9268.

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20

D'Alton, S., M. Altshuler, and J. Lewis. "Studies of alternative isoforms provide insight into TDP-43 autoregulation and pathogenesis." RNA 21, no. 8 (June 18, 2015): 1419–32. http://dx.doi.org/10.1261/rna.047647.114.

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21

Snijder, Eric J., Marjolein Kikkert, and Ying Fang. "Arterivirus molecular biology and pathogenesis." Journal of General Virology 94, no. 10 (October 1, 2013): 2141–63. http://dx.doi.org/10.1099/vir.0.056341-0.

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Arteriviruses are positive-stranded RNA viruses that infect mammals. They can cause persistent or asymptomatic infections, but also acute disease associated with a respiratory syndrome, abortion or lethal haemorrhagic fever. During the past two decades, porcine reproductive and respiratory syndrome virus (PRRSV) and, to a lesser extent, equine arteritis virus (EAV) have attracted attention as veterinary pathogens with significant economic impact. Particularly noteworthy were the ‘porcine high fever disease’ outbreaks in South-East Asia and the emergence of new virulent PRRSV strains in the USA. Recently, the family was expanded with several previously unknown arteriviruses isolated from different African monkey species. At the molecular level, arteriviruses share an intriguing but distant evolutionary relationship with coronaviruses and other members of the order Nidovirales. Nevertheless, several of their characteristics are unique, including virion composition and structure, and the conservation of only a subset of the replicase domains encountered in nidoviruses with larger genomes. During the past 15 years, the advent of reverse genetics systems for EAV and PRRSV has changed and accelerated the structure–function analysis of arterivirus RNA and protein sequences. These systems now also facilitate studies into host immune responses and arterivirus immune evasion and pathogenesis. In this review, we have summarized recent advances in the areas of arterivirus genome expression, RNA and protein functions, virion architecture, virus–host interactions, immunity, and pathogenesis. We have also briefly reviewed the impact of these advances on disease management, the engineering of novel candidate live vaccines and the diagnosis of arterivirus infection.

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22

Sznajder, Łukasz J., and Maurice S. Swanson. "Short Tandem Repeat Expansions and RNA-Mediated Pathogenesis in Myotonic Dystrophy." International Journal of Molecular Sciences 20, no. 13 (July 9, 2019): 3365. http://dx.doi.org/10.3390/ijms20133365.

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Short tandem repeat (STR) or microsatellite, expansions underlie more than 50 hereditary neurological, neuromuscular and other diseases, including myotonic dystrophy types 1 (DM1) and 2 (DM2). Current disease models for DM1 and DM2 propose a common pathomechanism, whereby the transcription of mutant DMPK (DM1) and CNBP (DM2) genes results in the synthesis of CUG and CCUG repeat expansion (CUGexp, CCUGexp) RNAs, respectively. These CUGexp and CCUGexp RNAs are toxic since they promote the assembly of ribonucleoprotein (RNP) complexes or RNA foci, leading to sequestration of Muscleblind-like (MBNL) proteins in the nucleus and global dysregulation of the processing, localization and stability of MBNL target RNAs. STR expansion RNAs also form phase-separated gel-like droplets both in vitro and in transiently transfected cells, implicating RNA-RNA multivalent interactions as drivers of RNA foci formation. Importantly, the nucleation and growth of these nuclear foci and transcript misprocessing are reversible processes and thus amenable to therapeutic intervention. In this review, we provide an overview of potential DM1 and DM2 pathomechanisms, followed by a discussion of MBNL functions in RNA processing and how multivalent interactions between expanded STR RNAs and RNA-binding proteins (RBPs) promote RNA foci assembly.

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23

Chi, Wang, Wang, Yu, and Yang. "Long Non-Coding RNA in the Pathogenesis of Cancers." Cells 8, no. 9 (September 1, 2019): 1015. http://dx.doi.org/10.3390/cells8091015.

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The incidence and mortality rate of cancer has been quickly increasing in the past decades. At present, cancer has become the leading cause of death worldwide. Most of the cancers cannot be effectively diagnosed at the early stage. Although there are multiple therapeutic treatments, including surgery, radiotherapy, chemotherapy, and targeted drugs, their effectiveness is still limited. The overall survival rate of malignant cancers is still low. It is necessary to further study the mechanisms for malignant cancers, and explore new biomarkers and targets that are more sensitive and effective for early diagnosis, treatment, and prognosis of cancers than traditional biomarkers and methods. Long non-coding RNAs (lncRNAs) are a class of RNA transcripts with a length greater than 200 nucleotides. Generally, lncRNAs are not capable of encoding proteins or peptides. LncRNAs exert diverse biological functions by regulating gene expressions and functions at transcriptional, translational, and post-translational levels. In the past decade, it has been demonstrated that the dysregulated lncRNA profile is widely involved in the pathogenesis of many diseases, including cancer, metabolic disorders, and cardiovascular diseases. In particular, lncRNAs have been revealed to play an important role in tumor growth and metastasis. Many lncRNAs have been shown to be potential biomarkers and targets for the diagnosis and treatment of cancers. This review aims to briefly discuss the latest findings regarding the roles and mechanisms of some important lncRNAs in the pathogenesis of certain malignant cancers, including lung, breast, liver, and colorectal cancers, as well as hematological malignancies and neuroblastoma.

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24

Bluml, S., M. Bonelli, B. Niederreiter, A. Puchner, G. Mayr, S. Hayer, M. I. Koenders, W. B. van den Berg, J. Smolen, and K. Redlich. "Micro-RNA 155 controls the pathogenesis of autoimmune arthritis." Annals of the Rheumatic Diseases 70, Suppl 2 (February 22, 2011): A79—A80. http://dx.doi.org/10.1136/ard.2010.149013.28.

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25

Gómez, Gustavo, Germán Martínez, and Vicente Pallás. "Interplay between viroid-induced pathogenesis and RNA silencing pathways." Trends in Plant Science 14, no. 5 (May 2009): 264–69. http://dx.doi.org/10.1016/j.tplants.2009.03.002.

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26

Lemmens, Robin, Melissa J. Moore, Ammar Al-Chalabi, Robert H. Brown, and Wim Robberecht. "RNA metabolism and the pathogenesis of motor neuron diseases." Trends in Neurosciences 33, no. 5 (May 2010): 249–58. http://dx.doi.org/10.1016/j.tins.2010.02.003.

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27

Michlewski, Gracjan, and Wlodzimierz Krzyzosiak. "Pathogenesis of spinocerebellar ataxias viewed from the RNA perspective." Cerebellum 4, no. 1 (April 2005): 19–24. http://dx.doi.org/10.1080/14734220510007905.

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28

Saksela, Kalle. "HIV4 RNA in Blood and Pathogenesis of HIV Infection." Annals of Medicine 27, no. 6 (January 1995): 625–28. http://dx.doi.org/10.3109/07853899509019247.

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29

Reed, Joanne H., and Tom P. Gordon. "Ro60-associated RNA takes its toll on disease pathogenesis." Nature Reviews Rheumatology 12, no. 3 (November 10, 2015): 136–38. http://dx.doi.org/10.1038/nrrheum.2015.148.

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30

Yang, Lu, and Hai Y. Liu. "Small RNA molecules in endometriosis: pathogenesis and therapeutic aspects." European Journal of Obstetrics & Gynecology and Reproductive Biology 183 (December 2014): 83–88. http://dx.doi.org/10.1016/j.ejogrb.2014.10.043.

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31

LaPointe, Autumn T., and Kevin J. Sokoloski. "De-Coding the Contributions of the Viral RNAs to Alphaviral Pathogenesis." Pathogens 10, no. 6 (June 19, 2021): 771. http://dx.doi.org/10.3390/pathogens10060771.

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Alphaviruses are positive-sense RNA arboviruses that are capable of causing severe disease in otherwise healthy individuals. There are many aspects of viral infection that determine pathogenesis and major efforts regarding the identification and characterization of virulence determinants have largely focused on the roles of the nonstructural and structural proteins. Nonetheless, the viral RNAs of the alphaviruses themselves play important roles in regard to virulence and pathogenesis. In particular, many sequences and secondary structures within the viral RNAs play an important part in the development of disease and may be considered important determinants of virulence. In this review article, we summarize the known RNA-based virulence traits and host:RNA interactions that influence alphaviral pathogenesis for each of the viral RNA species produced during infection. Overall, the viral RNAs produced during infection are important contributors to alphaviral pathogenesis and more research is needed to fully understand how each RNA species impacts the host response to infection as well as the development of disease.

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32

Kliuchnikova, AA, and SA Moshkovskii. "Adenosine-to-inosine RNA editing may be implicated in human pathogenesis." TARGETED ONCOTHERAPY, no. 2 (April 16, 2019): 22–25. http://dx.doi.org/10.24075/brsmu.2019.028.

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Adenosine-to-inosine (A-to-I) RNA editing is a common mechanism of post-transcriptional modification in many metazoans including vertebrates; the process is catalyzed by adenosine deaminases acting on RNA (ADARs). Using high-throughput sequencing technologies resulted in finding thousands of RNA editing sites throughout the human transcriptome however, their functions are still poorly understood. The aim of this brief review is to draw attention of clinicians and biomedical researchers to ADAR-mediated RNA editing phenomenon and its possible implication in development of neuropathologies, antiviral immune responses and cancer.

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33

Kerkvliet, Jason, Ramakrishna Edukulla, and Moses Rodriguez. "Novel Roles of the Picornaviral 3D Polymerase in Viral Pathogenesis." Advances in Virology 2010 (2010): 1–9. http://dx.doi.org/10.1155/2010/368068.

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The RNA-dependent RNA-polymerase,3Dpol, is an essential component in the picornavirus genome for the replication of single stranded RNA. However, transgenic expression of3Dpolin mice has antiviral effects. Here, we discuss the structure and function of3Dpolduring picornavirus replication, we review the evidence and consequence of a host immune response to epitopes in3Dpolafter picornavirus infection, highlight data showing the antiviral effects of transgenic3Dpolfrom Theiler's murine encephalomyelitis virus (TMEV), and discuss potential mechanisms by which3Dpolis causing this antiviral effect in mice.

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34

Alaqeel, AM, H. Abou Al-Shaar, RK Shariff, and A. Albakr. "The role of RNA metabolism in neurological diseases." Balkan Journal of Medical Genetics 18, no. 2 (December 1, 2015): 5–14. http://dx.doi.org/10.1515/bjmg-2015-0080.

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Abstract Neurodegenerative disorders are commonly encountered in medical practices. Such diseases can lead to major morbidity and mortality among the affected individuals. The molecular pathogenesis of these disorders is not yet clear. Recent literature has revealed that mutations in RNA-binding proteins are a key cause of several human neuronal-based diseases. This review discusses the role of RNA metabolism in neurological diseases with specific emphasis on roles of RNA translation and microRNAs in neurodegeneration, RNA-mediated toxicity, repeat expansion diseases and RNA metabolism, molecular pathogenesis of amyotrophic lateral sclerosis and frontotemporal dementia, and neurobiology of survival motor neuron (SMN) and spinal muscular atrophy.

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35

Locke, Marissa Christine, Alissa Young, Lindsey E. Cook, Kristen Monte, and Deborah Lenschow. "Investigating the pathogenesis of chronic chikungunya virus infection." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 171.6. http://dx.doi.org/10.4049/jimmunol.204.supp.171.6.

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Abstract Chikungunya virus (CHIKV) is an arthritogenic alphavirus that acutely causes fever as well as severe joint and muscle pain. Chronic musculoskeletal pain persists in a substantial fraction of patients for months to years after infection. While replicating virus is not detected in joint-associated tissues of patients nor in various animal models at convalescent time points, viral RNA is detected months after acute infection. To identify the cells that might contribute to chronic pathogenesis, we developed a recombinant CHIKV that expresses Cre recombinase (CHIKV-3′-Cre). CHIKV-3′-Cre infection of tdTomato reporter mice resulted in a population of tdTomato+ cells that persisted for at least 112 days. Immunofluorescence and flow cytometric profiling 28 days post infection revealed that these tdTomato+ cells were predominantly myofibers and fibroblasts as well as a small population of macrophages. Further, tdTomato+ cells are enriched for CHIKV RNA. Interestingly, the population of surviving cells was dynamic over time with macrophages making up a high percentage of the cells early and then tapering off. We applied this system to determine the differential roles of the type I interferon (IFN) subtypes during chronic CHIKV infection. Results using IFN blocking antibodies revealed that mice lacking the IFNαs, but not IFNβ, show an increase in chronic RNA levels and the number of fibroblasts that survive CHIKV infection in distal sites, indicating that type I IFNs have divergent roles during chronic CHIKV disease. Ongoing studies will explore the differential functions of IFNαs and IFNβ, will determine why the surviving cells and viral RNA are not cleared by the immune system, and will elucidate their contribution to chronic inflammation.

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36

Pauli, Cornelius, Michael Kienhöfer, Stefanie Göllner, and Carsten Müller-Tidow. "Epitranscriptomic modifications in acute myeloid leukemia: m⁶A and 2′-O-methylation as targets for novel therapeutic strategies." Biological Chemistry 402, no. 12 (October 11, 2021): 1531–46. http://dx.doi.org/10.1515/hsz-2021-0286.

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Анотація:

Abstract Modifications of RNA commonly occur in all species. Multiple enzymes are involved as writers, erasers and readers of these modifications. Many RNA modifications or the respective enzymes are associated with human disease and especially cancer. Currently, the mechanisms how RNA modifications impact on a large number of intracellular processes are emerging and knowledge about the pathogenetic role of RNA modifications increases. In Acute Myeloid Leukemia (AML), the N 6-methyladenosine (m6A) modification has emerged as an important modulator of leukemogenesis. The writer proteins METTL3 and METTL14 are both involved in AML pathogenesis and might be suitable therapeutic targets. Recently, close links between 2′-O-methylation (2′-O-me) of ribosomal RNA and leukemogenesis were discovered. The AML1-ETO oncofusion protein which specifically occurs in a subset of AML was found to depend on induction of snoRNAs and 2′-O-me for leukemogenesis. Also, NPM1, an important tumor suppressor in AML, was associated with altered snoRNAs and 2′-O-me. These findings point toward novel pathogenetic mechanisms and potential therapeutic interventions. The current knowledge and the implications are the topic of this review.

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37

K, Ghosh. "Covid19 the Virus Immunology and Blood Coagulation, a Positive Feedback Cycle with Resultant Pathogenesis: A Perspective." Virology & Immunology Journal 4, no. 3 (September 8, 2020): 1–3. http://dx.doi.org/10.23880/vij-16000251.

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Анотація:

Covid 19 is a new beta corona virus which is driving the present pandemic across the world. The virus is highly transmissible through respiratory route with a Ro value varying between1.3-2.0. The virus is a direct strand RNA virus and is one of the largest viruses of RNA virus group. It has 11 open reading frame of which ORF 9-11 is involved in translation of structural S (Spike), E (Envelop), M (Matrix) and N (Nucleocapsid) glycoproteins. Of these S protein is very important from the point of view of virus engagement with the host cell and its infectivity.

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38

Wilkinson, Emma, Yan-Hong Cui, and Yu-Ying He. "Context-Dependent Roles of RNA Modifications in Stress Responses and Diseases." International Journal of Molecular Sciences 22, no. 4 (February 16, 2021): 1949. http://dx.doi.org/10.3390/ijms22041949.

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Анотація:

RNA modifications are diverse post-transcriptional modifications that regulate RNA metabolism and gene expression. RNA modifications, and the writers, erasers, and readers that catalyze these modifications, serve as important signaling machineries in cellular stress responses and disease pathogenesis. In response to stress, RNA modifications are mobilized to activate or inhibit the signaling pathways that combat stresses, including oxidative stress, hypoxia, therapeutic stress, metabolic stress, heat shock, DNA damage, and ER stress. The role of RNA modifications in response to these cellular stressors is context- and cell-type-dependent. Due to their pervasive roles in cell biology, RNA modifications have been implicated in the pathogenesis of different diseases, including cancer, neurologic and developmental disorders and diseases, and metabolic diseases. In this review, we aim to summarize the roles of RNA modifications in molecular and cellular stress responses and diseases.

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39

Gao, Mengjia, Jingxin Xin, Xiaoling Li, Ling Gao, Shanshan Shao, and Meng Zhao. "Differential Expression Profiles of mRNA and Noncoding RNA and Analysis of Competitive Endogenous RNA Regulatory Networks in Nonalcoholic Steatohepatitis." Gastroenterology Research and Practice 2022 (July 7, 2022): 1–13. http://dx.doi.org/10.1155/2022/3200932.

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Nonalcoholic steatohepatitis (NASH) is a liver disease caused by multiple factors, and there is no approved pharmacotherapy. The pathogenesis of NASH remains underexplored. In this study, differentially expressed circular RNAs (circRNAs) were obtained by analyzing NASH-related circRNA datasets, and then, corresponding target microRNAs (miRNAs) and messenger RNAs (mRNAs) were predicted to construct a circRNA–miRNA–mRNA regulatory network. On this basis, a total of 38 circRNAs, 7 miRNAs, and 10 mRNAs were screened out. The present study reveals novel circRNA biomarkers of NASH and reports a potential competing endogenous RNA (ceRNA) regulatory network that might provide insights for further investigation into the underlying pathogenesis of NASH.

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40

Sieff, Colin A., and Harvey F. Lodish. "Pathogenesis of the Erythroid Failure in Diamond Blackfan Anemia." Blood 110, no. 11 (November 16, 2007): 424. http://dx.doi.org/10.1182/blood.v110.11.424.424.

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The discovery that several ribosomal protein genes can be mutated in DBA suggests that ribosomal protein gene mutations may account for many or all cases of DBA, and focuses attention on the ribosome. While experiments in yeast and recently in mammalian cells show that RPS19 depletion or mutation leads to a block in ribosomal RNA biosynthesis, this result does not explain why erythropoiesis is so severely affected in DBA. We hypothesize that during fetal development immature erythroid cells proliferate more rapidly than other lineages and therefore require very high ribosome synthetic rates to generate sufficient capacity for translation of erythroid specific transcripts that must take place before these unique cells enucleate; furthermore, we postulate that a block in ribosome biogenesis or reduced protein synthetic capacity that occurs in mutant DBA cells leads to loss of proliferation and cell death of rapidly dividing cells, but survival and normal differentiation of cells that are dividing more slowly, yielding fewer (macrocytic) erythrocytes. To test this kinetic hypothesis we infected primary mouse fetal liver cells with siRNAs to RPS19 and compared proliferation, differentiation, RNA biogenesis and cell cycle status in wild type and knockdown cells. Mouse fetal liver cells were double-labeled for erythroid-specific TER119 and non erythroid-specific transferrin receptor (CD71) and analyzed by flow-cytometry. E14.5 fetal livers contain at least five distinct populations of cells, defined by their characteristic staining patterns. We purified the most primitive progenitor cells by depletion of mature TER119high cells. During a two-day period the number of erythroblasts increases 15-30 fold, corresponding to 4–5 cell divisions, which correlates well with the number of terminal cell divisions that a CFU-E goes through to generate terminally differentiated erythrocytes. The progenitor cells divide twice during the first 24 hours in erythropoietin (EPO); during the next 24 hours on fibronectin but no EPO, differentiated cells are produced in another 2–3 divisions. The retrovirus infected siRNA RPS19 knockdown cells show reduced proliferation of FACS sorted GFP positive cells at 48 hours. Although the cell yield is reduced, the differentiation pattern of the surviving GFP positive cells is similar to that of the controls. We next measured RNA content of wild type cells at 0, 24 and 48 hours. During the first 24 hours cell number increases 3–4 fold; remarkably, there is a 6-fold increase in RNA content during the same period, suggesting that the cells accumulate an excess of ribosomal RNA (80% of measured RNA) during early erythropoiesis. This was confirmed by quantitative real time PCR of rRNA. From 24–48 hours the cells decrease in size as they mature, and RNA yield per cell decreases; however, cell number increases markedly so the net effect is that total RNA in the culture plateaus or decreases. Because the siRNAs are not expressed until 24–48 hours, we modified the culture system to allow expansion without differentiation of immature cells in EPO, IGF-1 and dexamethasone. Under these conditions proliferation in siRNA expressing precursors is reduced. Cell cycle analysis shows a reduced proportion of cells in G1 or S phase and an increase in G2/M in the knockdown cells. Taken together, these data suggest that RPS19 insufficient erythroid cells proliferate poorly because of inadequate accumulation of ribosome synthetic capacity. The surviving cells differentiate normally but slowly, giving rise to macrocytes. In conclusion, kinetic considerations can explain the erythroid deficiency in DBA.

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41

Hofmann, Jeffrey W., William W. Seeley, and Eric J. Huang. "RNA Binding Proteins and the Pathogenesis of Frontotemporal Lobar Degeneration." Annual Review of Pathology: Mechanisms of Disease 14, no. 1 (January 24, 2019): 469–95. http://dx.doi.org/10.1146/annurev-pathmechdis-012418-012955.

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Frontotemporal dementia is a group of early onset dementia syndromes linked to underlying frontotemporal lobar degeneration (FTLD) pathology that can be classified based on the formation of abnormal protein aggregates involving tau and two RNA binding proteins, TDP-43 and FUS. Although elucidation of the mechanisms leading to FTLD pathology is in progress, recent advances in genetics and neuropathology indicate that a majority of FTLD cases with proteinopathy involving RNA binding proteins show highly congruent genotype–phenotype correlations. Specifically, recent studies have uncovered the unique properties of the low-complexity domains in RNA binding proteins that can facilitate liquid–liquid phase separation in the formation of membraneless organelles. Furthermore, there is compelling evidence that mutations in FTLD genes lead to dysfunction in diverse cellular pathways that converge on the endolysosomal pathway, autophagy, and neuroinflammation. Together, these results provide key mechanistic insights into the pathogenesis and potential therapeutic targets of FTLD.

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42

Zhang, Q. B., Y. Q. Huang, F. N. Xiao, G. L. Jian, Y. P. Tang, F. Dai, J. X. Zheng, and Y. F. Qing. "POS1146 NONCODING RNA CONTRIBUTE TO PATHOGENESIS IN PRIMARY GOUTY ARTHRITIS." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 852.1–852. http://dx.doi.org/10.1136/annrheumdis-2021-eular.4056.

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Background:Gout is an arthritic disease caused by the deposition of monosodium urate crystal (MSU) in the joints, which can lead to acute inflammation and damage adjacent tissue [1].Over the past decade, noncoding RNAs (ncRNAs) have been shown to have crucial importance in health and disease[2,3]. However, studies evaluating the function of ncRNAs in gout are scarce, and current knowledge of the role of ncRNAs in gout is still limited.Objectives:To assess the contribution of noncoding RNAs to gout and the clinical importance of these genes in primary gouty arthritis (GA).Methods:The mRNA expression levels of noncoding RNAs (LINC00173, LINC00963, LINC01330 and miRNA-182-5p) were measured in peripheral blood mononuclear cells (PBMCs) from 60 gout patients(including 30 acute gout patients, 30 intercritical gout patients) and 40 healthy subjects. The relationship between noncoding RNA expression levels and laboratory features was analyzed in GA patients.Results:The expression levels of LINC00173, LINC00963 and miRNA-182-5p were much lower in the AG and IG group than in the HC groups (p<0.05), and no significant difference was detected between AG and IG groups(P>0.05). The expression levels of LINC01330 were much lower in the AG group than in the IG and HC groups (p<0.05), and no significant difference was detected between AG and IG groups(P>0.05). In GA patients, the levels of noncoding RNAs mRNA correlated with laboratory inflammatory and metabolic indexes.Conclusion:Altered noncoding RNAs expression suggests that noncoding RNAs is involved in the pathogenesis of GA and participates in regulating inflammation and metabolism.References:[1]Xu Yi-Ting,Leng Ying-Rong,Liu Ming-Ming et al. MicroRNA and long noncoding RNA involvement in gout and prospects for treatment.[J].Int Immunopharmacol, 2020, 87: 106842.doi:10.1016/j.intimp.2020.106842[2]Yu Yunfang,Zhang Wenda,Li Anlin et al. Association of Long Noncoding RNA Biomarkers With Clinical Immune Subtype and Prediction of Immunotherapy Response in Patients With Cancer.[J].JAMA Netw Open, 2020, 3: e202149.doi:10.1001/jamanetworkopen.2020.2149[3]Zou Yaoyao,Xu Siqi,Xiao Youjun et al. Long noncoding RNA LERFS negatively regulates rheumatoid synovial aggression and proliferation.[J].J Clin Invest, 2018, 128: 4510-4524.doi:10.1172/JCI97965Figure 1.Relative Expression of noncoding RNAs in the PBMCs of Patients.Disclosure of Interests:Quan-Bo Zhang Grant/research support from: the National Natural Science Foundation of China(General Program) (no.81974250) and Science and Technology Plan Project of Sichuan Province (no.2018JY0257), Yu-Qin Huang: None declared, Fan-Ni Xiao: None declared, gui-lin jian: None declared, Yi-Ping Tang: None declared, Fei Dai: None declared, Jian-Xiong Zheng: None declared, Yu-Feng Qing Grant/research support from: Science and Technology Project of Nanchong City (no.18SXHZ0522).

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43

Xing, E., A. C. Billi, L. Tsoi, and J. E. Gudjonsson. "692 Interrogating mechanisms of granuloma annulare pathogenesis through RNA sequencing." Journal of Investigative Dermatology 141, no. 5 (May 2021): S120. http://dx.doi.org/10.1016/j.jid.2021.02.722.

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44

Camarena, Laura, Vincent Bruno, Ghia Euskirchen, Sebastian Poggio, and Michael Snyder. "Molecular Mechanisms of Ethanol-Induced Pathogenesis Revealed by RNA-Sequencing." PLoS Pathogens 6, no. 4 (April 1, 2010): e1000834. http://dx.doi.org/10.1371/journal.ppat.1000834.

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45

Mastroyiannopoulos, Nikolas P., Christos Shammas, and Leonidas A. Phylactou. "Tackling the pathogenesis of RNA nuclear retention in myotonic dystrophy." Biology of the Cell 102, no. 9 (September 2010): 515–23. http://dx.doi.org/10.1042/bc20100040.

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46

Tagawa, Hiroyuki, Sho Ikeda, and Kenichi Sawada. "Role of micro RNA in the pathogenesis of malignant lymphoma." Cancer Science 104, no. 7 (April 29, 2013): 801–9. http://dx.doi.org/10.1111/cas.12160.

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47

Abduljalil, Jameel M. "Bacterial riboswitches and RNA thermometers: Nature and contributions to pathogenesis." Non-coding RNA Research 3, no. 2 (June 2018): 54–63. http://dx.doi.org/10.1016/j.ncrna.2018.04.003.

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48

Zhang, Wei, Weiting Xu, Yu Feng, and Xiang Zhou. "Non‐coding RNA involvement in the pathogenesis of diabetic cardiomyopathy." Journal of Cellular and Molecular Medicine 23, no. 9 (June 26, 2019): 5859–67. http://dx.doi.org/10.1111/jcmm.14510.

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49

Liu, Nuo, Zhen-Zhen Wang, Ming Zhao, Yi Zhang, and Nai-Hong Chen. "Role of non-coding RNA in the pathogenesis of depression." Gene 735 (April 2020): 144276. http://dx.doi.org/10.1016/j.gene.2019.144276.

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50

Jiang, Nan, Wenwei Pan, Jinhui Li, Tiefeng Cao, and Huimin Shen. "Upregulated Circular RNA hsa_circ_0008433 Regulates Pathogenesis in Endometriosis Via miRNA." Reproductive Sciences 27, no. 11 (June 16, 2020): 2002–17. http://dx.doi.org/10.1007/s43032-020-00219-1.

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