Correction: Gan, L.; Denecke, B. Profiling Pre-MicroRNA and Mature MicroRNA Expressions Using a Single Microarray and Avoiding Separate Sample Preparation. Microarrays 2013, 2, 24-33.
Ontology highlight
ABSTRACT:
SUBMITTER: Gan L
PROVIDER: S-EPMC5003463 | biostudies-literature | 2013 Jun
REPOSITORIES: biostudies-literature
Publications
Correction: Gan, L.; Denecke, B. Profiling Pre-MicroRNA and Mature MicroRNA Expressions Using a Single Microarray and Avoiding Separate Sample Preparation. Microarrays 2013, 2, 24-33.
Microarrays (Basel, Switzerland) 20130624 3
It came to our attention that a paper has recently been published concerning one of the GEO datasets (GSE34413) we cited in our published paper [1]. The original reference (reference 27) cited for this dataset leads to a paper about a similar study from the same research group [2]. In order to provide readers with exact citation information, we would like to update reference 27 in our previous paper to the new published paper concerning GSE34413 [3]. The authors apologize for this inconvenience. ...[more]
Similar Datasets
Project description:Mature microRNA is a crucial component in the gene expression regulation network. At the same time, microRNA gene expression and procession is regulated in a precise and collaborated way. Pre-microRNAs mediate products during the microRNA transcription process, they can provide hints of microRNA gene expression regulation or can serve as alternative biomarkers. To date, little effort has been devoted to pre-microRNA expression profiling. In this study, three human and three mouse microRNA profile data sets, based on the Affymetrix miRNA 2.0 array, have been re-analyzed for both mature and pre-microRNA signals as a primary test of parallel mature/pre-microRNA expression profiling on a single platform. The results not only demonstrated a glimpse of pre-microRNA expression in human and mouse, but also the relationship of microRNA expressions between pre- and mature forms. The study also showed a possible application of currently available microRNA microarrays in profiling pre-microRNA expression in a time and cost effective manner.
| S-EPMC5003435 | biostudies-literature
Project description:Microarray technology has become a very popular approach in cases where multiple experiments need to be conducted repeatedly or done with a variety of samples. In our lab, we are applying our high density spots microarray approach to microscopy visualization of the effects of transiently introduced siRNA or cDNA on cellular morphology or phenotype. In this publication, we are discussing the possibility of using this micro-scale high throughput process to study the role of microRNAs in the biology of selected cellular models. After reverse-transfection of microRNAs and siRNA, the cellular phenotype generated by microRNAs regulated NF-κB expression comparably to the siRNA. The ability to print microRNA molecules for reverse transfection into cells is opening up the wide horizon for the phenotypic high content screening of microRNA libraries using cellular disease models.
| S-EPMC5003479 | biostudies-literature
Project description:Recent deep-learning techniques have made it possible to manipulate facial expressions in digital photographs or videos, however, these techniques still lack fine and personalized ways to control their creation. Moreover, current technologies are highly dependent on large labeled databases, which limits the range and complexity of expressions that can be modeled. Thus, these technologies cannot deal with non-basic emotions. In this paper, we propose a novel interdisciplinary approach combining the Generative Adversarial Network (GAN) with a technique inspired by cognitive sciences, psychophysical reverse correlation. Reverse correlation is a data-driven method able to extract an observer's 'mental representation' of what a given facial expression should look like. Our approach can generate 1) personalized facial expression prototypes, 2) of basic emotions, and non-basic emotions that are not available in existing databases, and 3) without the need for expertise. Personalized prototypes obtained with reverse correlation can then be applied to manipulate facial expressions. In addition, our system challenges the universality of facial expression prototypes by proposing the concepts of dominant and complementary action units to describe facial expression prototypes. The evaluations we conducted on a limited number of emotions validate the effectiveness of our proposed method. The code is available at https://github.com/yansen0508/Mental-Deep-Reverse-Engineering.
| S-EPMC10456187 | biostudies-literature
Project description:BackgroundBecause of the central functions of the mitochondria in providing metabolic energy and initiating apoptosis on one hand and the role that microRNA (miRNA) play in gene expression, we hypothesized that some miRNA could be present in the mitochondria for post-transcriptomic regulation by RNA interference. We intend to identify miRNA localized in the mitochondria isolated from human skeletal primary muscular cells.Methodology/principal findingsTo investigate the potential origin of mitochondrial miRNA, we in-silico searched for microRNA candidates in the mtDNA. Twenty five human pre-miRNA and 33 miRNA aligments (E-value<0.1) were found in the reference mitochondrial sequence and some of the best candidates were chosen for a co-localization test. In situ hybridization of pre-mir-302a, pre-let-7b and mir-365, using specific labelled locked nucleic acids and confocal microscopy, demonstrated that these miRNA were localized in mitochondria of human myoblasts. Total RNA was extracted from enriched mitochondria isolated by an immunomagnetic method from a culture of human myotubes. The detection of 742 human miRNA (miRBase) were monitored by RT-qPCR at three increasing mtRNA inputs. Forty six miRNA were significantly expressed (2(nd) derivative method Cp>35) for the smallest RNA input concentration and 204 miRNA for the maximum RNA input concentration. In silico analysis predicted 80 putative miRNA target sites in the mitochondrial genome (E-value<0.05).Conclusions/significanceThe present study experimentally demonstrated for the first time the presence of pre-miRNA and miRNA in the human mitochondria isolated from skeletal muscular cells. A set of miRNA were significantly detected in mitochondria fraction. The origin of these pre-miRNA and miRNA should be further investigate to determine if they are imported from the cytosol and/or if they are partially processed in the mitochondria.
| S-EPMC3102686 | biostudies-literature
Project description:BackgroundMicroRNAs are known to be generated from primary transcripts mainly through the sequential cleavages by two enzymes, Drosha and Dicer. The sequence of a mature microRNA, especially the 'seeding sequence', largely determines its binding ability and specificity to target mRNAs. Therefore, methods that predict mature microRNA sequences with high accuracy will benefit the identification and characterization of novel microRNAs and their targets, and contribute to inferring the post-transcriptional regulation network at a genome scale.Methodology/principal findingsWe have developed a method, MiRmat, to predict the mature microRNA sequence. MiRmat is essentially composed of two parts: the prediction of Drosha processing site and the identification of Dicer processing site. Based on the analysis of microRNAs from 12 species, we found that the patterns of free energy profiles are conserved among vertebrate microRNA hairpins. Therefore, we introduced in our method the free energy distribution pattern of the downstream part of pri-microRNA secondary structure and Random Forest algorithm to predict the mature microRNA sequence. Based on the evaluation on an independent test dataset from 10 vertebrates, MiRmat was shown to identify 77.8% of the Drosha processing sites and 92.8% of the Dicer sites within a deviation of 2 nt. In a more stringent evaluation by excluding the microRNAs sharing the same family between the training set and test set, MiRmat kept a rather well performance of 71.9% and 87.2% of the identification rate on the Drosha and Dicer site respectively, which represents the ability to deal with the novel microRNA family. MiRmat outperforms other state-of-the-art methods and has a high degree of efficacy for the prediction of mature microRNA sequences of vertebrates.ConclusionMiRmat was developed for identifying microRNA mature sequence(s) by introducing the free energy distribution of RNA stem-loop structure and the Random Forest algorithm. We prove that MiRmat has better performance than the existing tools and is applicable among vertebrates. MiRmat is freely available at http://mcube.nju.edu.cn/jwang/lab/soft/MiRmat/.
| S-EPMC3531441 | biostudies-literature
Project description:ObjectiveDefective autophagy in macrophages leads to pathological processes that contribute to atherosclerosis, including impaired cholesterol metabolism and defective efferocytosis. Autophagy promotes the degradation of cytoplasmic components in lysosomes and plays a key role in the catabolism of stored lipids to maintain cellular homeostasis. microRNA-33 (miR-33) is a post-transcriptional regulator of genes involved in cholesterol homeostasis, yet the complete mechanisms by which miR-33 controls lipid metabolism are unknown. We investigated whether miR-33 targeting of autophagy contributes to its regulation of cholesterol homeostasis and atherogenesis.Approach and resultsUsing coherent anti-Stokes Raman scattering microscopy, we show that miR-33 drives lipid droplet accumulation in macrophages, suggesting decreased lipolysis. Inhibition of neutral and lysosomal hydrolysis pathways revealed that miR-33 reduced cholesterol mobilization by a lysosomal-dependent mechanism, implicating repression of autophagy. Indeed, we show that miR-33 targets key autophagy regulators and effectors in macrophages to reduce lipid droplet catabolism, an essential process to generate free cholesterol for efflux. Notably, miR-33 regulation of autophagy lies upstream of its known effects on ABCA1 (ATP-binding cassette transporter A1)-dependent cholesterol efflux, as miR-33 inhibitors fail to increase efflux upon genetic or chemical inhibition of autophagy. Furthermore, we find that miR-33 inhibits apoptotic cell clearance via an autophagy-dependent mechanism. Macrophages treated with anti-miR-33 show increased efferocytosis, lysosomal biogenesis, and degradation of apoptotic material. Finally, we show that treating atherosclerotic Ldlr-/- mice with anti-miR-33 restores defective autophagy in macrophage foam cells and plaques and promotes apoptotic cell clearance to reduce plaque necrosis.ConclusionsCollectively, these data provide insight into the mechanisms by which miR-33 regulates cellular cholesterol homeostasis and atherosclerosis.
| S-EPMC5494696 | biostudies-literature
Project description:CCL2-mediated macrophage infiltration in articular tissues plays a pivotal role in the development of the osteoarthritis (OA). miRNAs regulate the onset and progression of diseases via controlling the expression of a series of genes. How the CCL2 gene was regulated by miRNAs was still not fully elucidated. In the present study, we demonstrated that the binding sites of miR-33 in the 3'UTR of CCL2 gene were conserved in human, mouse and rat species. By performing gain- or loss-of-function studies, we verified that miR-33 suppressed CCL2 expression in the mRNA and protein levels. We also found that miR-33 suppressed the CCL2 levels in the supernatant of cultured primary mouse chondrocytes. With reporter gene assay, we demonstrated that miR-33 targeted at AAUGCA in the 3'UTR of CCL2 gene. In transwell migration assays, we demonstrated that the conditional medium (CM) from miR-33 deficient chondrocytes potentiated the monocyte chemotaxis in a CCL2 dependent manner. Finally, we demonstrated that the level of miR-33 was decreased, whereas the CCL2 level was increased in the articular cartilage from the OA patients compared with the control group. In summary, we identified miR-33 as a novel suppressor of CCL2 in chondrocytes. The miR-33/CCL2 axis in chondrocytes regulates monocyte chemotaxis, providing a potential mechanism of macrophage infiltration in OA.
| S-EPMC4859085 | biostudies-other
Project description:Although Argonaute (AGO) proteins have been the focus of microRNA (miRNA) studies, we observed AGO-free mature miRNAs directly interacting with RNA-binding proteins, implying the sophisticated nature of fine-tuning gene regulation by miRNAs. To investigate microRNA-binding proteins (miRBPs) globally, we analyzed PAR-CLIP data sets to identify RBP quaking (QKI) as a novel miRBP for let-7b. Potential existence of AGO-free miRNAs were further verified by measuring miRNA levels in genetically engineered AGO-depleted human and mouse cells. We have shown that QKI regulates miRNA-mediated gene silencing at multiple steps, and collectively serves as an auxiliary factor empowering AGO2/let-7b-mediated gene silencing. Depletion of QKI decreases interaction of AGO2 with let-7b and target mRNA, consequently controlling target mRNA decay. This finding indicates that QKI is a complementary factor in miRNA-mediated mRNA decay. QKI, however, also suppresses the dissociation of let-7b from AGO2, and slows the assembly of AGO2/miRNA/target mRNA complexes at the single-molecule level. We also revealed that QKI overexpression suppresses cMYC expression at post-transcriptional level, and decreases proliferation and migration of HeLa cells, demonstrating that QKI is a tumour suppressor gene by in part augmenting let-7b activity. Our data show that QKI is a new type of RBP implicated in the versatile regulation of miRNA-mediated gene silencing.
| S-EPMC10878027 | biostudies-literature
Project description:Innate immunity plays a prominent role in the host defense against pathogens and must be precisely regulated. As vital orchestrators in cholesterol homeostasis, microRNA-33/33* have been widely investigated in cellular metabolism. However, their role in antiviral innate immunity is largely unknown. Here, we report that VSV stimulation decreased the expression of miR-33/33* through an IFNAR-dependent manner in macrophages. Overexpression of miR-33/33* resulted in impaired RIG-I signaling, enhancing viral load and lethality whereas attenuating type I interferon production both in vitro and in vivo. In addition, miR-33/33* specifically prevented the mitochondrial adaptor mitochondrial antiviral-signaling protein (MAVS) from forming activated aggregates by targeting adenosine monophosphate activated protein kinase (AMPK), subsequently impeding the mitophagy-mediated elimination of damaged mitochondria and disturbing mitochondrial homeostasis which is indispensable for efficient MAVS activation. Our findings establish miR-33/33* as negative modulators of the RNA virus-triggered innate immune response and identify a previously unknown regulatory mechanism linking mitochondrial homeostasis with antiviral signaling pathways.
| S-EPMC8167167 | biostudies-literature
Project description:Argonaute (AGO), a component of RNA-induced silencing complexes (RISCs), is a representative RNA-binding protein (RBP) known to bind with mature microRNAs (miRNAs) and is directly involved in post-transcriptional gene silencing. However, despite the biological significance of miRNAs, the roles of other miRNA-binding proteins (miRBPs) remain unclear in the regulation of miRNA loading, dissociation from RISCs and extracellular release. In this study, we performed protein arrays to profile miRBPs and identify 118 RBPs that directly bind to miRNAs. Among those proteins, the RBP quaking (QKI) inhibits extracellular release of the mature microRNA let-7b by controlling the loading of let-7b into extracellular vesicles via additional miRBPs such as AUF1 (also known as hnRNPD) and hnRNPK. The enhanced extracellular release of let-7b after QKI depletion activates Toll-like receptor 7 (TLR7) and promotes the production of proinflammatory cytokines in recipient cells, leading to brain inflammation in the mouse cortex. Thus, this study reveals the contribution of QKI to the inhibition of brain inflammation via regulation of extracellular let-7b release.
| S-EPMC11574364 | biostudies-literature