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The microRNA miR-21 is a mediator of FGF8 action on cortical COUP-TFI translation

ABSTRACT: These data support a translational control of COUP-TFI gradient expression by FGF8 via miR-21 and contribute to our understanding of how regionalized expression is established during neocortical area mapping

ORGANISM(S): Mus musculus

PROVIDER: GSE117932 | GEO | 2018/08/01

REPOSITORIES: GEO

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The microRNA miR-21 is a mediator of FGF8 action on cortical COUP-TFI translation

Project description:The microRNA miR-21 is a mediator of FGF8 action on cortical COUP-TFI translation

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Wild-type and COUP-TFI-/- newborn inner ear microarrays

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The microRNA miR-21 Is a Mediator of FGF8 Action on Cortical COUP-TFI Translation.

Project description:The morphogen FGF8 plays a pivotal role in neocortical area patterning through its inhibitory effect on COUP-TFI/Nr2f1 anterior expression, but its mechanism of action is poorly understood. We established an in vitro model of mouse embryonic stem cell corticogenesis in which COUP-TFI protein expression is inhibited by the activation of FGF8 in a time window corresponding to cortical area patterning. Interestingly, overexpression of the COUP-TFI 3'UTR reduces the inhibitory effect of FGF8 on COUP-TFI translation. FGF8 induces the expression of few miRNAs targeting COUP-TFI 3'UTR in silico. We found that the functional inhibition of miR-21 can effectively counteract the inhibitory effect of FGF8 in vitro and regulate COUP-TFI protein levels in vivo. Accordingly, miR-21 expression is complementary to COUP-TFI expression during corticogenesis. These data support a translational control of COUP-TFI gradient expression by FGF8 via miR-21 and contribute to our understanding of how regionalized expression is established during neocortical area mapping.

| S-EPMC6135738 | biostudies-literature

ChIP-seq analysis of COUP-TFI enrichment in neural retina.

Project description:The genome-wide binding sites of COUP-TFI in neural retina.

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Wild-type and COUP-TFI-/- newborn inner ear microarrays

Project description:In order to establish a list of candidate direct COUP-TFI gene targets in the inner ear, we analyzed the differential gene expression profiles of the wild-type and the COUP-TFIâ/â P0 inner ears. We performed a total of 8 microarray experiments using Affymetrix MG-U74Av2 chips, including 2 biological and 2 experimental replicates per genotype sample. Due to limiting RNA yields from the newborn inner ear, each microarray chip was hybridized with an RNA pool from multiple tissue samples. We analyzed our data using two different algorithms: GC-Robust Multi-Array (GCRMA) and dChip. Each normalized expression dataset was subsequently analyzed by 2-way ANOVA, evaluating both genotype and experimental effects. This statistical approach allowed us to 1) account for an experimental effect observed in the expression value of many genes, therefore increasing the power of the analysis, and 2) filter out potential expression differences due to contamination during dissections (contaminating genes would present as probes with a significant interaction p-value). Using this methodology, the gene hits from the GCRMA-normalized expression dataset consisted of 256 genes with a significant genotype effect (p<0.01) and no interaction (p>0.01). Similar cutoffs applied on the dChip-normalized dataset resulted in 250 significant gene hits. Within both groups, COUP-TFI has the lowest genotype p-value, validating our statistical approach.

2010-06-08 | E-GEOD-16744 | biostudies-arrayexpress

ChIP-seq analysis of COUP-TFI enrichment in neural retina.

Project description:ChIP-seq analysis of COUP-TFI enrichment in neural retina.

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Orphan nuclear receptor COUP-TFII enhances myofibroblasts glycolysis leading to kidney fibrosis

Project description:Recent studies demonstrated that metabolic disturbance, such as augmented glycolysis, contributes to fibrosis. The molecular regulation of this metabolic perturbation in fibrosis, however, has been elusive. COUP-TFII (also known as NR2F2) is an important regulator of glucose and lipid metabolism. Its contribution to organ fibrosis is undefined. Here, we found increased COUP-TFII expression in myofibroblasts in human fibrotic kidneys, lungs, kidney organoids, and mouse kidneys after injury. Genetic ablation of COUP-TFII in mice resulted in attenuation of injury-induced kidney fibrosis. A non-biased proteomic study revealed the suppression of fatty acid oxidation and the enhancement of glycolysis pathways in COUP-TFII overexpressing fibroblasts. Overexpression of COUP-TFII in fibroblasts induced augmented glycolysis and production of alpha smooth muscle actin (αSMA) and collagen1. Knockout of COUP-TFII decreased glycolysis and collagen1 levels in fibroblasts. Chip-qPCR revealed the binding of COUP-TFII on the promoter of PGC1α. Overexpression of COUP-TFII reduced the cellular level of PGC1α. Targeting COUP-TFII serves as a novel treatment approach for mitigating fibrosis in chronic kidney disease and potentially fibrosis in other organs.

2021-04-27 | PXD024035 | Pride

Genes regulated by COUP-TFII inhibitor

Project description:The orphan nuclear receptor COUP-TFII is expressed at a low level in adult tissues, but its expression is increased and shown to promote progression of multiple diseases including prostate cancer, heart failure and muscular dystrophy. Suppression of COUP-TFII slows disease progression, making it an intriguing therapeutic target. Here, we identified a potent and specific COUP-TFII inhibitor through high-throughput screening. The inhibitor specifically suppressed COUP-TFII activity to regulate its target genes.

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Expression profile of COUP-TFII overexpressing hearts

Project description:Increased COUP-TFII levels are found in human dilated cardiomyopathy as well as in mouse models that develop cardiomyopathy. COUP-TFII overexpression in adult mouse hearts caused ventricular dilation and compromised cardiac functions. To gain insights on COUP-TFII’s effect in hearts, we identified the molecular profile of COUP-TFII overexpressing hearts through microarray analysis. The result may shred light on molecular mechanisms that mediate development of dilated cardiomyopathy.

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Expression profile of COUP-TFII overexpressing mouse ventral midbrain

Project description:Elevated COUP-TFII levels are found in Parkinson’s disease. COUP-TFII overexpression in mouse dopaminergic neurons caused neurodegeneration. The goal of this study is to identify molecular mechanisms of COUP-TFII-mediated cell death through RNAseq.

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