1,723,481 research outputs found
DataSheet_1_Promotor Hypomethylation Mediated Upregulation of miR-23b-3p Targets PTEN to Promote Bronchial Epithelial-Mesenchymal Transition in Chronic Asthma.pdf
No full textChronic asthma is characterized by airway inflammation and irreversible airway remodeling. Epithelial-mesenchymal transition (EMT) is a typical pathological change of airway remodeling. Our previous research demonstrated miR-23b inhibited airway smooth muscle proliferation while the function of miR-23b-3p has not been reported yet. Besides, miRNA is regulated by many factors, including DNA methylation. The function of miR-23b-3p and whether it is regulated by DNA methylation are worth exploring. Balb/c mice were given OVA sensitization to develop the asthmatic model. Expression of miR-23b-3p and EMT markers were measured by RT-qPCR, WB and immunohistochemistry (IHC). DNA methylation was detected by methylation-specific PCR (MSP) and the MassARRAY System. Asthmatic mice and TGF-β1-stimulated bronchial epithelial cells (BEAS-2B) showed EMT with increased miR-23b-3p. Overexpression of miR-23b-3p promoted EMT and migration, while inhibition of miR-23b-3p reversed these transitions. DNA methyltransferases were decreased in asthmatic mice. MSP and MassARRAY System detected the promotor of miR-23b showed DNA hypomethylation. DNA methyltransferase inhibitor 5’-AZA-CdZ increased the expression of miR-23b-3p. Meanwhile, PTEN was identified as a target gene of miR-23b-3p. Our results indicated that promotor hypomethylation mediated upregulation of miR-23b-3p targets PTEN to promote EMT in chronic asthma. miR-23b-3p and DNA methylation might be potential therapeutic targets for irreversible airway remodeling.</p
Lamp1 is a target of Mir-23b-3p in macrophage.
No full text(A) Four different databases were used to cross-predict mir-23b-3p targets and 26 potential targets presented in Venn. (B) The bioinformatics prediction of mir-23a/b-3p MRE in Lamp1. (C) Luciferase reporter assay was performed in 293T cells co-transfected with pmirGLO-Lamp1-Wt or Mut and mimics or mimics-NC in Raw264.7 cells. (D) RT-qPCR was performed to examine the expression of Lamp1 in Raw264.7 cells transfected with mimics-NC, mimics, inhibitor-NC, or inhibitor.</p
Additional file 1 of Knockdown of lncRNA PVT1 alleviates high glucose-induced proliferation and fibrosis in human mesangial cells by miR-23b-3p/WT1 axis
No full textAdditional file 1: Fig. S1. The correlation between PVT1 and miR-23b-3p or WT1 was detected using the RNA pulldown or RIP assays. (A) RNA pulldown assay for the correlation between PVT1 and miR-23b-3p using bio-NC, bio-miR-23b-3p-WT or bio-miR-23b-3p-MUT. (B) RIP assays for the correlation between miR-23b-3p and WT1 using anti-Ago2 or anti-IgG antibody. *P < 0.05
MicroRNA miR-23b-3p promotes osteosarcoma by targeting ventricular zone expressed PH domain-containing 1 (VEPH1)/phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway
No full textIncreasing evidence suggests that dysregulated miRNA expression can lead to the tumorigenesis of osteosarcoma (OS). Nevertheless, the potential role of miR-23b-3p in OS is unclear and remains to be explored. Microarray analysis was performed to identify key genes involved in OS. Reverse transcription quantitative polymerase chain reaction and Western blotting were used to examine miR-23b-3p expression, ventricular zone expressed PH domain-containing 1 (VEPH1) transcript (as well as other transcripts as indicated), and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway-related protein expression. A luciferase reporter gene assay was performed to confirm the regulatory relationship between VEPH1 mRNA and miR-23b-3p. Cell viability was evaluated using the Cell Counting Kit-8 assay, cell growth was assessed using the bromodeoxyuridine enzyme-linked immunosorbent assay, and cell migration was tested using a wound healing assay. We found significant upregulation of miR-23b-3p in OS, which prominently promoted the viability, proliferation, and migration of OS cells. Additionally, VEPH1 was found to be a target of miR-23b-3p and its expression was decreased in OS. Lastly, VEPH1 alleviated the promotion effect of miR-23b-3p on the malignancy phenotypes of OS cells via the PI3K/AKT signaling pathway. Thus, miR-23b-3p augmented the viability, proliferation, and migration of OS cells by directly targeting and downregulating VEPH1, which inhibited the activation of the PI3K/AKT signaling pathway.</p
Additional file 4 of Human mesenchymal stem cells derived exosomes inhibit the growth of acute myeloid leukemia cells via regulating miR-23b-5p/TRIM14 pathway
No full textAdditional file 4: Fig. S4. The expression of miR-23b-5p after the application of miR-23b-5p mimic and inhibitor. *** p < 0.001
Data_Sheet_1_Circulating plasma miR-23b-3p as a biomarker target for idiopathic Parkinson's disease: comparison with small extracellular vesicle miRNA.docx
No full textBackgroundParkinson's disease (PD) is an increasingly common neurodegenerative condition, which causes movement dysfunction and a broad range of non-motor symptoms. There is no molecular or biochemical diagnosis test for PD. The miRNAs are a class of small non-coding RNAs and are extensively studied owing to their altered expression in pathological states and facile harvesting and analysis techniques.MethodsA total of 48 samples (16 each of PD, aged-matched, and young controls) were recruited. The small extracellular vesicles (sEVs) were isolated and validated using Western blot, transmission electron microscope, and nanoparticle tracking analysis. Small RNA isolation, library preparation, and small RNA sequencing followed by differential expression and targeted prediction of miRNA were performed. The real-time PCR was performed with the targeted miRNA on PD, age-matched, and young healthy control of plasma and plasma-derived sEVs to demonstrate their potential as a diagnostic biomarker.ResultsIn RNA sequencing, we identified 14.89% upregulated (fold change 1.11 to 11.04, p ConclusionWe observed an opposite expression profile of miR-23b-3p in PD and age-matched healthy control in plasma and plasma-derived sEV fractions, where the expression of miR-23b-3p is increased in PD plasma while decreased in plasma-derived sEV fractions. We further observed the different miR-23b-3p expression profiles in young and age-matched healthy control.</p
Pneumococcal 23B Molecular Subtype Identified Using Whole Genome Sequencing
No full textThe polysaccharide capsule is a major virulence factor of Streptococcus pneumoniae and the target of all currently licensed pneumococcal vaccines. At present, there are 92 serologically distinct pneumococcal serotypes. Structural and antigenic variation of capsular types is the result of genetic variation within the capsular polysaccharide synthesis (CPS) locus; however, genetic variation may not always result in phenotypic differences which produce novel serotypes. With the introduction of high throughput whole genome sequencing, discovery of novel genotypic variants is not unexpected and this study describes a novel variant of the serotype 23B CPS operon. This novel variant was characterized as a novel genotypic subtype (23B1) with ∼70% homology to the published 23B CPS sequence. High sequence variability was determined in eight cps genes involved in sugar biosynthesis. However, there was no distinction between the classic 23B serotype and 23B1 serologically or in terms of polysaccharide structure. Phylogenetic and eBURST analysis revealed a distinct lineage for 23B1 with multiple clones (UK, Thailand, and USA) that arose at different points during pneumococcal evolution. Analysis of the UK S. pneumoniae isolates (n = 121) revealed an upsurge of 23B1 ST2372 in 2011, after which this previously unseen ST increased to reach 50% proportion of the 23B sequenced isolates from 2013 and remained prevalent within our sequenced isolates from later years. Therefore, although the 23B1 variant appears to have no phenotypic impact and cannot be considered as novel serotype, it appears to have led to a genetic restructuring of the UK serotype 23B population
MiR-23b/
No full text<p>-<b>27b significantly increases E-cadherin expression in castration –resistant cell lines.</b> ALVA31 or PC3-ML cells expressing miR-23b/-27b or transduced with scrambled control and LNCaP cells transfected with antagomiR-23b/-27b or control antagomiR were subjected to western blotting for E-cadherin and actin. Representative blots are shown of a total of 2–6 experiments.</p
MiR-23b/
No full text<p>-<b>27b expression decreases the invasiveness of castration-resistant prostate cancer cells while inhibition of miR-23b/</b>-<b>27b in androgen-dependent prostate cancer cells increases invasiveness.</b> A, Matrigel invasion assays were performed on ALVA31 cells (A) and PC3-ML cells (B) expressing miR-23b/-27b or scrambled control-transduced cells. Upper panels show representative regions of the chamber filters with crystal violet-stained cells. The fold change (±SEM) represents the number of invaded cells per chamber divided by controls from three independent experiments performed in triplicate for A and the means (±SD) of one independent experiment done in triplicate for B (***P<0.001). C, LNCaP cells were transfected with 50 nM control antagomiR or antagomiR-23b/-27b. Matrigel invasion assays were performed 72 hours post transfection as explained above. The means (±SD) of two independent experiments performed in triplicate are shown (***P<0.001).</p
Suppression of miR-23b by anti-miR-23b oligonucleotides enhances glioma cell migration.
No full text<p><b>A.</b> Effect of anti-miR-23b on miR-23b expression. T98G glioma cells were transfected with 100 nM anti-miR-23b oligonucleotide or a random sequence control oligonucleotide. 48 hours after transfection, expression of miR-23b was determined by quantitative PCR. <b>B</b> pre-coated with 10 µg/ml human laminin 16 hours after transfection. Cell migration was ass<b>.</b> Effect of anti-miR-23b expression on glioma migration. Cells were seeded onto 10-well glass slides essed over 24 hr. Bars represents the average of three independent experiments (*: <i>p</i><0.05).</p
- …
