miRWalk2.0: a comprehensive atlas of microRNA-target interactions

Dweep, Harsh; Gretz, Norbert

doi:10.1038/nmeth.3485

Cited by 1,191 publications

(964 citation statements)

References 4 publications

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“…First, putative target genes of dysregulated miRNAs were predicted using the miRWalk 2.0 algorithm 25. Databases for predicted target genes consisted of miRanda,26 RNA22,27 and Targetscan,28 as well as miRWalk 2.0 25.…”

Section: Methodsmentioning

confidence: 99%

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Maternal immune activation alters brain microRNA expression in mouse offspring

Sunwoo

Jeon²,

Moon

et al. 2018

Ann Clin Transl Neurol

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ObjectiveMaternal immune activation (MIA) is associated with an increased risk of autism spectrum disorder (ASD) in offspring. Herein, we investigate the altered expression of microRNAs (miRNA), and that of their target genes, in the brains of MIA mouse offspring.MethodsTo generate MIA model mice, pregnant mice were injected with polyriboinosinic:polyribocytidylic acid on embryonic day 12.5. We performed miRNA microarray and mRNA sequencing in order to determine the differential expression of miRNA and mRNA between MIA mice and controls, at 3 weeks of age. We further identified predicted target genes of dysregulated miRNAs, and miRNA‐target interactions, based on the inverse correlation of their expression levels.ResultsMice prenatally subjected to MIA exhibited behavioral abnormalities typical of ASD, such as a lack of preference for social novelty and reduced prepulse inhibition. We found 29 differentially expressed miRNAs (8 upregulated and 21 downregulated) and 758 differentially expressed mRNAs (542 upregulated and 216 downregulated) in MIA offspring compared to controls. Based on expression levels of the predicted target genes, 18 downregulated miRNAs (340 target genes) and three upregulated miRNAs (60 target genes) were found to be significantly enriched among the differentially expressed genes. miRNA and target gene interactions were most significant between mmu‐miR‐466i‐3p and Hfm1 (ATP‐dependent DNA helicase homolog), and between mmu‐miR‐877‐3p and Aqp6 (aquaporin 6).InterpretationOur results provide novel information regarding miRNA expression changes and their putative targets in the early postnatal period of brain development. Further studies will be needed to evaluate potential pathogenic roles of the dysregulated miRNAs.

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Section: Methodsmentioning

confidence: 99%

“…Databases for predicted target genes consisted of miRanda,26 RNA22,27 and Targetscan,28 as well as miRWalk 2.0 25. Putative target genes were identified when the miRNA‐target interactions were verified by three or more databases.…”

Section: Methodsmentioning

confidence: 99%

Maternal immune activation alters brain microRNA expression in mouse offspring

Sunwoo

Jeon²,

Moon

et al. 2018

Ann Clin Transl Neurol

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“…Children with low miR-375 had increased Th2 cytokines (IL-5 and IL-13) and mast-cell specific gene (CPA3 and TPSAB1) expression. Based on miRWalk2.0's predictive algorithm, miR-375 is not expected to bind to IL-5, IL-13, CPA3 and TPSAB1 [34] . As a result, these Th2 cytokines are unlikely to be the direct targets of miR-375 activity and unlikely to constitute the mechanism by which miR-375 regulates esophageal inflammation.…”

Section: Mir-375 Deficiency In Esophageal Epithelium Of Eoe Patientsmentioning

confidence: 99%

“…As a result, these Th2 cytokines are unlikely to be the direct targets of miR-375 activity and unlikely to constitute the mechanism by which miR-375 regulates esophageal inflammation. It seems more likely based on predictive algorithms that miR-375 regulates JAK2, a critical intercellular member of JAK/STAT-mediated cytokine signaling pathways [34] . Studies by Lu et al [31,32] and Zahm et al [33] all similarly identify a deficiency of miR-375 in diseased esophageal tissue that could, in theory, relieve inhibition on JAK2 and promote increased signaling of Th2 cytokine pathways [ Figure 3].…”

Section: Mir-375 Deficiency In Esophageal Epithelium Of Eoe Patientsmentioning

confidence: 99%

Biomarkers and therapeutic targets: microRNA roles in the pathophysiology, diagnosis and management of eosinophilic esophagitis

Lambert

Jhaveri²,

Jhaveri

2018

JTGG

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How to cite this article: Lambert KA, Jhaveri P, Jhaveri P. Biomarkers and therapeutic targets: microRNA roles in the pathophysiology, AbstractEosinophilic esophagitis (EoE) is a chronic inflammatory disease that is increasingly recognized as the cause of common gastrointestinal symptoms including dysphagia, chest and abdominal pain, heartburn, food impaction, and food refusal in children and adults. Often referred to as "asthma of the esophagus", eosinophilic esophagitis, like its asthma counterpart, is an allergic disorder on the rise worldwide. Clinically managed by food avoidance, steroid therapy, recurring endoscopic evaluations and dilations as needed, eosinophilic esophagitis is a poorly understood disease process with limited therapies and even fewer diagnostic tools to predict and surveil active inflammation. As a result, there is a critical need to identify noninvasive biomarkers and therapeutic targets for eosinophilic esophagitis. Here we review the known contributions of miRNAs to eosinophilic inflammation of the esophagus and the potential for miRNA biomarkers for EoE in the clinical setting.

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“…miRNAs targeting FSHR were predicted using three algorithms: TargetScan (Lewis et al 2003), miRWalk (Dweep & Gretz 2015), and miRanda (Enright et al 2003). The mature sequences of miR-126* genes from multiple vertebrate species were downloaded from miRBase (http://www.mirbase.org) and the GenBank database (http://www.ncbi.nlm.nih.gov), and sequence alignment was performed using ClustalW (http:// www.ebi.…”

Section: Bioinformatic Analysesmentioning

confidence: 99%

Androgen receptor and miRNA-126* axis controls follicle-stimulating hormone receptor expression in porcine ovarian granulosa cells

Du¹,

Pan²,

Li³

2016

Reproduction

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Androgen, which acts via the androgen receptor (AR), plays crucial roles in mammalian ovarian function. Recent studies showed that androgen/AR signaling regulates follicle-stimulating hormone receptor (FSHR) expression in follicles; however, the detailed mechanism underlying this regulation remained unknown. Here, we demonstrate that AR and miR-126* cooperate to inhibit FSHR expression and function in pig follicular granulosa cells (pGCs). In pGCs, overexpression of AR decreased, whereas knockdown increased, FSHR mRNA and protein expression; however, neither manipulation affected FSHR promoter activity. Using a dualluciferase reporter assay, we found that the FSHR gene is a direct target of miR-126*, which inhibits FSHR expression and increases the rate of AR-induced apoptosis in pGCs. Collectively, our data show for the first time that the AR/miR-126* axis exerts synergetic effects in the regulation of FSHR expression and apoptosis in pGCs. Our findings thus define a novel pathway, AR/miR-126*/FSHR, that regulates mammalian GC functions.Reproduction (2016) 152 161-169

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miRWalk2.0: a comprehensive atlas of microRNA-target interactions

Cited by 1,191 publications

References 4 publications

Maternal immune activation alters brain microRNA expression in mouse offspring

Maternal immune activation alters brain microRNA expression in mouse offspring

Biomarkers and therapeutic targets: microRNA roles in the pathophysiology, diagnosis and management of eosinophilic esophagitis

Androgen receptor and miRNA-126* axis controls follicle-stimulating hormone receptor expression in porcine ovarian granulosa cells

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