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    The miR-590 C57T SNP reduces levels of miR-590-5p and miR-590-3p, without affecting the levels of pri-miR-590 and pre-miR-590.

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    (A) Quantification of pri-miR-590 by qRT-PCR normalized by GAPDH. Mean ± SD (n = 3). HEK293T cells were transfected with the pri-miR-590-WT or pri-miR-590-SNP plasmids. The empty plasmid was used as negative control. (B-F) Northern blot images for pre-miRNA, miRNA, and U6 RNA using total RNA prepared from HEK293T cells transfected with the pri-miR-590-WT or pri-miR-590-SNP plasmids. The empty plasmid was used as negative control. Four biological replicates were analyzed for each transfection plasmid. Northern probes used are perfectly complementary to miR-590-5p (A), miR-590-3p-WT (B), miR-590-3p-SNP (C), miR-16-5p (D), and U6 RNA (E). The miR-590-3p-WT probe weakly cross-hybridized to miR-590-3p-SNP, and vice versa. (G) The abundance of pre-miR-590, miR-590-5p and miR-590-3p-(WT/SNP) relative to the mean value of miR-590-5p in the WT miR-590 gene plasmid transfection conditions. (H) The abundance of miR-16-5p normalized to the mean value of the pri-miR-590-WT plasmid transfection conditions. Mean ± SD (n = 4).</p

    Supplementary Material for: miR-590-3p Is a Novel MicroRNA in Myocarditis by Targeting Nuclear Factor Kappa-B in vivo

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    Objective: Nuclear factor kappa-B (NF-κB)-induced inflammation leads to myocarditis and heart dysfunction. How microRNAs (miRNAs) contribute to this process is poorly defined. The aim of this study was to investigate whether miRNAs regulate NF-κB-induced inflammation in experimental autoimmune myocarditis (EAM) in vivo. Methods and Results: NF-κB and its related proinflammatory genes, including interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a), were activated in EAM. Profiling of NF-κB-related miRNAs revealed that miR-590-3p was strikingly reduced in EAM. We found IL-6-induced proinflammatory signaling via miR-590-3p reduction, p50 induction, NF-κB activation and IL-6/TNF-a expression. Moreover, a luciferase reporter assay demonstrated that miR-590-3p directly interacted with the 3' UTR (untranslated region) of the p50 subunit, and that miR-590-3p overexpression inhibited p50 expression. Finally, miR-590-3p transfection through adeno-associated virus significantly inhibited p50 expression, suppressed NF-κB activity and blocked IL-6/TNF-a expression in vivo, reducing the lesion area and improving cardiac function in EAM. Conclusion: miR-590-3p is a novel NF-κB-related miRNA that directly targets the p50 subunit. This may provide a novel strategy for the treatment of myocarditis

    Additional file 1 of Functional role and epithelial to mesenchymal transition of the miR-590-3p/MDM2 axis in hepatocellular carcinoma

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    Additional file 1: Figure S1. miR-590-3p directly targets EMT-TF SLUG, ZEB1, and ZEB2 in HCC, as determined by bioinformatics analysis (A) CSmiRTar database analysis showing SLUG, ZEB1 and ZEB2 as miR-590-3p potential target genes. (B) TargetScan analysis showing the sequence alignment between the seed region of miR-50-3p and its downstream target genes. Although SNAIL was not predicted as a direct target of miR-590-3p by CSmiRTar database or TargetScan, we observed a marked reduction in the transcript levels of SNAIL using RT-qPCR analysis, suggesting that miR-590-3p may target SNAIL through other players primarily regulated by miR-590-3p, such as MDM2. * SNAI2= SLUG

    Additional file 2 of Functional role and epithelial to mesenchymal transition of the miR-590-3p/MDM2 axis in hepatocellular carcinoma

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    Additional file 2: Figure S2. Sequence alignment between miR-590-3p and N-cadherin but not Vimentin. TargetScan shows that the mesenchymal marker N-cadherin harbours three different binding sites with miR-590-3p in its 3′UTR, while no binding was shown with the other tested mesenchymal marker, Vimentin, supporting the notion that miR-590-3p suppresses EMT through directly regulating N-cadherin, while it might be that there is an indirect regulation on Vimentin hindering the early detection of the change in its levels, that is why it was not detected in our analysis

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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