Identifying microRNAs and Their Editing Sites in Macaca mulatta

Wang, Qingyi; Zhao, Zhigang; Zhang, Xiaotuo; Lu, Chenyu; Ren, Shuchao; Li, Shipeng; Guo, Junqiang; Liao, Peiran; Jiang, Bingbing; Zheng, Yun

doi:10.3390/cells8070682

Cited by 11 publications

(16 citation statements)

References 67 publications

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“…After statistical analysis of nucleotides besides these A-to-I editing sites, we found that the 5' and 3' end of these A-to-I editing sites preferred to be U and G (Fig. 2b), respectively, which was also noticed in previous studies 36,47,48,62 . As examples, MiRME maps of hsa-mir-1301 and hsa-mir-539 in one of the prefrontal cortex and frontal cortex samples (SRR1759213 and SRR2287868, respectively) were presented in Figs.…”

supporting

confidence: 84%

MicroRNA editing patterns in Huntington’s disease

Guo

Yang

Jiang

et al. 2022

Sci Rep

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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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supporting

confidence: 84%

MicroRNA editing patterns in Huntington’s disease

Guo

Yang

Jiang

et al. 2022

Sci Rep

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“…2a). Similar to previous results [3,4,17,18], the 5’ and 3’ side of these A-to-I editing sites preferred to be U and G, respectively (ED: Fig. 2b).…”

Section: Resultssupporting

confidence: 90%

“…3a and Table S2.5). Five of these 26 C-to-U editing sites are conserved in primates [18] (see ED: Fig. 3a).…”

Section: Resultsmentioning

confidence: 99%

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Characterizing relevant microRNA editing sites in Parkinson’s disease

Ren

Zhao

et al. 2020

Preprint

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MicroRNAs (miRNAs) are extensively edited in human brains. However, the functional relevance of miRNA editome is largely unknown in Parkinson's disease (PD). By analyzed small RNA sequencing profiles of brain tissues of 43 PD patients and 88 normal controls, we totally identified 421 miRNA editing sites with significantly different editing levels in prefrontal cortices of PD patients (PD-PC). A-to-I edited miR-497-5p has significantly higher expression levels in PD-PC compared to normal controls and directly represses OPA1 and VAPB, which potentially contributes to the progressive neurodegeneration of PD patients. These results provide new insights into mechanistic understanding, novel diagnostic and therapeutic clues of PD. Introduction MicroRNAs (miRNAs) are small non-coding RNAs with about 22 nucleotides that normally repress their target mRNAs at post-transcriptional level [1]. Some miRNAs are edited, such as Adenosine-to-Inosine (A-to-I) editing [2-7] performed by adenosine deaminase (ADAR) enzymes and C-to-U editing performed by apolipoprotein B mRNA editing catalytic polypeptidelike (APOBEC) enzymes [8], during their biogenesis processes. Altered editing of miRNAs lead to human diseases, such as cancer [9-11]. Parkinson's disease is a neurodegenetative disorder affecting 2-3% of people over 65 years of age [12]. However the functional relevance of miRNA editing in PD is largely unknown, although A-to-I editing is prevalent in brain [13][14][15][16] and the editing level is gradually increasing in the developmental procedure [5,16].To comprehensively characterize miRNA editing sites in brain tissues of PD, we analyzing 43 and 88 small RNA sequencing profiles of PD and control brain tissues, respectively. We identified 421 miRNA editing sites that have significantly different editing levels in prefrontal cortices of PD patients (PD-PC) compared with control group. The editing levels of 6 Ato-I and 3 C-to-U editing sites are significantly correlated with the ages of normal controls which is disrupted in PD patients. One A-to-I editing site in miR-497-5p has significantly higher editing levels compared to normal controls in PD-PC samples and edited miR-497-5p directly represses OPA1 and VAPB, which potentially contributes to the progressive neurodegeneration of PD patients. These results demonstrate that miRNA editing is severely disturbed and relevant in PD and offer novel insight into the etiology of PD. The editing of miRNAs might be used to develop novel diagnostic biomarkers and/or therapeutic targets for PD.

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“…The angiopoietin (ANGPT) family is an important group of factors, specific for vascular endothelium, whose functions are mediated through two tyrosine kinase receptors, Tie1 and Tie2 [7]. The ANGPT-Tie ligand-receptor system exerts a key role in regulating vascular integrity [8,9].…”

Section: Introductionmentioning

confidence: 99%

Angiopoietins, Vascular Endothelial Growth Factors and Secretory Phospholipase A2 in Ischemic and Non-Ischemic Heart Failure

Varricchi

Loffredo

Bencivenga

et al. 2020

JCM

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Heart failure (HF) is a growing public health burden, with high prevalence and mortality rates. In contrast to ischemic heart failure (IHF), the diagnosis of non-ischemic heart failure (NIHF) is established in the absence of coronary artery disease. Angiopoietins (ANGPTs), vascular endothelial growth factors (VEGFs) and secretory phospholipases A2 (sPLA2s) are proinflammatory mediators and key regulators of endothelial cells. In the present manuscript, we analyze the plasma concentrations of angiogenic (ANGPT1, ANGPT2, VEGF-A) and lymphangiogenic (VEGF-C, VEGF-D) factors and the plasma activity of sPLA2 in patients with IHF and NIHF compared to healthy controls. The concentrations of ANGPT1, ANGPT2 and their ratio significantly differed between HF patients and healthy controls. Similarly, plasma levels of VEGF-D and sPLA2 activity were higher in HF as compared to controls. Concentrations of ANGPT2 and the ANGPT2/ANGPT1 ratio (an index of vascular permeability) were increased in NIHF patients. VEGF-A and VEGF-C concentrations did not differ among the three examined groups. Interestingly, VEGF-D was selectively increased in IFH patients compared to controls. Plasma activity of sPLA2 was increased in IHF and NIHF patients compared to controls. Our results indicate that several regulators of vascular permeability and smoldering inflammation are specifically altered in IHF and NIHF patients. Studies involving larger cohorts of these patients will be necessary to demonstrate the clinical implications of our findings.

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Identifying microRNAs and Their Editing Sites in Macaca mulatta

Cited by 11 publications

References 67 publications

MicroRNA editing patterns in Huntington’s disease

MicroRNA editing patterns in Huntington’s disease

Characterizing relevant microRNA editing sites in Parkinson’s disease

Angiopoietins, Vascular Endothelial Growth Factors and Secretory Phospholipase A2 in Ischemic and Non-Ischemic Heart Failure

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