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MicroRNA editing patterns in Huntington’s disease
Huntington’s disease (HD) is a neurodegenerative disease. MicroRNAs (miRNAs) are small non-coding RNAs that mediate post-transcriptional regulation of target genes. Although miRNAs are extensively edited in human brains, the editome of miRNAs in brains of HD patients is largely unknown. By analyzing...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8873361/ https://www.ncbi.nlm.nih.gov/pubmed/35210471 http://dx.doi.org/10.1038/s41598-022-06970-6 |
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author | Guo, Shiyong Yang, Jun Jiang, Bingbing Zhou, Nan Ding, Hao Zhou, Guangchen Wu, Shuai Suo, Angbaji Wu, Xingwang Xie, Wenping Li, Wanran Liu, Yulong Deng, Wei Zheng, Yun |
author_facet | Guo, Shiyong Yang, Jun Jiang, Bingbing Zhou, Nan Ding, Hao Zhou, Guangchen Wu, Shuai Suo, Angbaji Wu, Xingwang Xie, Wenping Li, Wanran Liu, Yulong Deng, Wei Zheng, Yun |
author_sort | Guo, Shiyong |
collection | PubMed |
description | Huntington’s disease (HD) is a neurodegenerative disease. MicroRNAs (miRNAs) are small non-coding RNAs that mediate post-transcriptional regulation of target genes. Although miRNAs are extensively edited in human brains, the editome of miRNAs in brains of HD patients is largely unknown. By analyzing the small RNA sequencing profiles of brain tissues of 28 HD patients and 83 normal controls, 1182 miRNA editing sites with significant editing levels were identified. In addition to 27 A-to-I editing sites, we identified 3 conserved C-to-U editing sites in miRNAs of HD patients. 30 SNPs in the miRNAs of HD patients were also identified. Furthermore, 129 miRNA editing events demonstrated significantly different editing levels in prefrontal cortex samples of HD patients (HD-PC) when compared to those of healthy controls. We found that hsa-mir-10b-5p was edited to have an additional cytosine at 5’-end in HD-PC, and the edited hsa-mir-10b repressed GTPBP10 that was often downregulated in HD. The down-regulation of GTPBP10 might contribute to the progression of HD by causing gradual loss of function of mitochondrial. These results provide the first endeavor to characterize the miRNA editing events in HD and their potential functions. |
format | Online Article Text |
id | pubmed-8873361 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-88733612022-02-25 MicroRNA editing patterns in Huntington’s disease Guo, Shiyong Yang, Jun Jiang, Bingbing Zhou, Nan Ding, Hao Zhou, Guangchen Wu, Shuai Suo, Angbaji Wu, Xingwang Xie, Wenping Li, Wanran Liu, Yulong Deng, Wei Zheng, Yun Sci Rep Article Huntington’s disease (HD) is a neurodegenerative disease. MicroRNAs (miRNAs) are small non-coding RNAs that mediate post-transcriptional regulation of target genes. Although miRNAs are extensively edited in human brains, the editome of miRNAs in brains of HD patients is largely unknown. By analyzing the small RNA sequencing profiles of brain tissues of 28 HD patients and 83 normal controls, 1182 miRNA editing sites with significant editing levels were identified. In addition to 27 A-to-I editing sites, we identified 3 conserved C-to-U editing sites in miRNAs of HD patients. 30 SNPs in the miRNAs of HD patients were also identified. Furthermore, 129 miRNA editing events demonstrated significantly different editing levels in prefrontal cortex samples of HD patients (HD-PC) when compared to those of healthy controls. We found that hsa-mir-10b-5p was edited to have an additional cytosine at 5’-end in HD-PC, and the edited hsa-mir-10b repressed GTPBP10 that was often downregulated in HD. The down-regulation of GTPBP10 might contribute to the progression of HD by causing gradual loss of function of mitochondrial. These results provide the first endeavor to characterize the miRNA editing events in HD and their potential functions. Nature Publishing Group UK 2022-02-24 /pmc/articles/PMC8873361/ /pubmed/35210471 http://dx.doi.org/10.1038/s41598-022-06970-6 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Guo, Shiyong Yang, Jun Jiang, Bingbing Zhou, Nan Ding, Hao Zhou, Guangchen Wu, Shuai Suo, Angbaji Wu, Xingwang Xie, Wenping Li, Wanran Liu, Yulong Deng, Wei Zheng, Yun MicroRNA editing patterns in Huntington’s disease |
title | MicroRNA editing patterns in Huntington’s disease |
title_full | MicroRNA editing patterns in Huntington’s disease |
title_fullStr | MicroRNA editing patterns in Huntington’s disease |
title_full_unstemmed | MicroRNA editing patterns in Huntington’s disease |
title_short | MicroRNA editing patterns in Huntington’s disease |
title_sort | microrna editing patterns in huntington’s disease |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8873361/ https://www.ncbi.nlm.nih.gov/pubmed/35210471 http://dx.doi.org/10.1038/s41598-022-06970-6 |
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