{"title":"LncRNA UCA1可通过调节miR-135a-5p调节神经性疼痛的进展","authors":"Bingbing Wu, Xiaogang Zhou","doi":"10.1016/j.mrfmmm.2023.111833","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Neuropathic pain<span><span> (NPP) is known as a common neurological disease with high incidence rate. The present work focused on the roles of long non-coding RNA </span>urothelial carcinoma antigen 1(LncRNA UCA1) in NPP and the possible underlying mechanism.</span></p></div><div><h3>Methods</h3><p>NPP rat model has been established and the levels of UCA1 NPP as well as the group has been determined by RT-PCR method. Next, NPP rats were treated by UCA1 over-expression plasmid and the behaviors, as well as expression of inflammatory cytokines have been examined. Furthermore, target miRNA of UCA1, miR-135a-5p, has been predicted by bioinformatic method, and further verified with the dual-luciferase reporter assay. Finally, the effects of UCA1/ miR-135a-5p axis have been further evaluated.</p></div><div><h3>Results</h3><p>Expressions of UCA1 were markedly decreased and miR-135a-5p were significantly increased in NPP rats in comparison with the control rats. Over-expression of UCA1 alleviated the inflammatory condition in NPP model by decreasing expression of inflammatory cytokines. miR-135a-5p was confirmed to be a target microRNA of UCA1, and UCA1 may regulate the progress of NPP via targeting miR-135a-5p.</p></div><div><h3>Conclusion</h3><p>UCA1 could regulate NPP via affecting miR-135a-5p expression.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"827 ","pages":"Article 111833"},"PeriodicalIF":1.5000,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LncRNA UCA1 could regulate the progression of neuropathic pain by regulating miR-135a-5p\",\"authors\":\"Bingbing Wu, Xiaogang Zhou\",\"doi\":\"10.1016/j.mrfmmm.2023.111833\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>Neuropathic pain<span><span> (NPP) is known as a common neurological disease with high incidence rate. The present work focused on the roles of long non-coding RNA </span>urothelial carcinoma antigen 1(LncRNA UCA1) in NPP and the possible underlying mechanism.</span></p></div><div><h3>Methods</h3><p>NPP rat model has been established and the levels of UCA1 NPP as well as the group has been determined by RT-PCR method. Next, NPP rats were treated by UCA1 over-expression plasmid and the behaviors, as well as expression of inflammatory cytokines have been examined. Furthermore, target miRNA of UCA1, miR-135a-5p, has been predicted by bioinformatic method, and further verified with the dual-luciferase reporter assay. Finally, the effects of UCA1/ miR-135a-5p axis have been further evaluated.</p></div><div><h3>Results</h3><p>Expressions of UCA1 were markedly decreased and miR-135a-5p were significantly increased in NPP rats in comparison with the control rats. Over-expression of UCA1 alleviated the inflammatory condition in NPP model by decreasing expression of inflammatory cytokines. miR-135a-5p was confirmed to be a target microRNA of UCA1, and UCA1 may regulate the progress of NPP via targeting miR-135a-5p.</p></div><div><h3>Conclusion</h3><p>UCA1 could regulate NPP via affecting miR-135a-5p expression.</p></div>\",\"PeriodicalId\":49790,\"journal\":{\"name\":\"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis\",\"volume\":\"827 \",\"pages\":\"Article 111833\"},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2023-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0027510723000209\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0027510723000209","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
LncRNA UCA1 could regulate the progression of neuropathic pain by regulating miR-135a-5p
Background
Neuropathic pain (NPP) is known as a common neurological disease with high incidence rate. The present work focused on the roles of long non-coding RNA urothelial carcinoma antigen 1(LncRNA UCA1) in NPP and the possible underlying mechanism.
Methods
NPP rat model has been established and the levels of UCA1 NPP as well as the group has been determined by RT-PCR method. Next, NPP rats were treated by UCA1 over-expression plasmid and the behaviors, as well as expression of inflammatory cytokines have been examined. Furthermore, target miRNA of UCA1, miR-135a-5p, has been predicted by bioinformatic method, and further verified with the dual-luciferase reporter assay. Finally, the effects of UCA1/ miR-135a-5p axis have been further evaluated.
Results
Expressions of UCA1 were markedly decreased and miR-135a-5p were significantly increased in NPP rats in comparison with the control rats. Over-expression of UCA1 alleviated the inflammatory condition in NPP model by decreasing expression of inflammatory cytokines. miR-135a-5p was confirmed to be a target microRNA of UCA1, and UCA1 may regulate the progress of NPP via targeting miR-135a-5p.
Conclusion
UCA1 could regulate NPP via affecting miR-135a-5p expression.
期刊介绍：
Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs.
MR publishes articles in the following areas:
Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence.
The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance.
Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing.
Landscape of somatic mutations and epimutations in cancer and aging.
Role of de novo mutations in human disease and aging; mutations in population genomics.
Interactions between mutations and epimutations.
The role of epimutations in chromatin structure and function.
Mitochondrial DNA mutations and their consequences in terms of human disease and aging.
Novel ways to generate mutations and epimutations in cell lines and animal models.
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