MicroRNA editing patterns in Huntington’s disease

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作者
Shiyong Guo
Jun Yang
Bingbing Jiang
Nan Zhou
Hao Ding
Guangchen Zhou
Shuai Wu
Angbaji Suo
Xingwang Wu
Wenping Xie
Wanran Li
Yulong Liu
Wei Deng
Yun Zheng
机构
[1] Kunming University of Science and Technology,State Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine
[2] Physical Evidence Spectral Technology Innovation Team,Faculty of Information Engineering and Automation
[3] Yunnan Police College,Center of Statistical Research
[4] Kunming University of Science and Technology,undefined
[5] Southwestern University of Finance and Economics,undefined
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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.
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