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Illumina array to compare whole-genome expression change in miR-127 KO mice at E18.5 in 3 tissues: brain, skin and muscle

ABSTRACT: miR-127 is an imprinted microRNA on mouse chromosome 12, strongly expressed during late embryogenesis and known regulator of placental gene Rtl1. miR-127-knockout (KO) mice appear phenotypically normal. An Illumina beadchip whole genome microarray experiment was carried out on embryonic stage 18.5 (E18.5) mice with a deletion in the miR-127 gene, and compared with wild type (WT) mice. Three tissues with varying expression of miR-127 were analysed: brain, skin and muscle. For each tissue (brain, skin, muscle) and genotype (WT or miR-127 KO), total RNA from 15 different embryos was extracted. These RNA samples were divided into three pools of five, to make three biological replicates. Each biological replicate was applied to two separate Illumina Mouse WG-6 v2.0 beadchips, to make two technical replicates.

ORGANISM(S): Mus musculus

SUBMITTER: Sarah Allen

PROVIDER: E-GEOD-47110 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Illumina array to compare whole-genome expression change in miR-127 KO mice at E18.5 in 3 tissues: brain, skin and muscle

Project description:miR-127 is an imprinted microRNA on mouse chromosome 12, strongly expressed during late embryogenesis and known regulator of placental gene Rtl1. miR-127-knockout (KO) mice appear phenotypically normal. An Illumina beadchip whole genome microarray experiment was carried out on embryonic stage 18.5 (E18.5) mice with a deletion in the miR-127 gene, and compared with wild type (WT) mice. Three tissues with varying expression of miR-127 were analysed: brain, skin and muscle.

2014-05-20 | GSE47110 | GEO

Genome-wide analysis of gene expression changes in miR-214 KO mouse hearts and skeletal muscle

Project description:Early reperfusion of ischemic cardiac tissue remains the most effective intervention for improving clinical outcome following myocardial infarction. However, abrupt increases in intracellular Ca2+ during myocardial reperfusion cause cardiomyocyte death and consequent loss of cardiac function, referred to as ischemia/reperfusion (IR) injury. Cardiac IR is accompanied by dynamic changes in expression of microRNAs (miRNAs), which inhibit specific mRNA targets. miR-214 is up-regulated during ischemic injury and heart failure in mice and humans, but its potential role in these processes is unknown. We show that genetic deletion of miR-214 in mice causes loss of cardiac contractility, increased apoptosis, and excessive fibrosis in response to IR injury. The microarray contains 6 samples, each containing cDNA pooled from 3 mice per group. There are no replicates. The array was designed to make 3 different pairwise comparisons between the following: P14 WT and miR-214 KO hearts; adult WT and miR-214 KO skeletal muscle; adult WT and miR-214 KO hearts

2012-01-31 | E-GEOD-35421 | biostudies-arrayexpress

Human Alopecia Areata Skin Profiling

Project description:Our goal was to develop a transcriptomic description of affected alopecic scalp skin from patients with alopecia areata. 5 biological replicates of skin samples from 5 separate AA patients compared with 5 similar scalp samples from healthy control patients

2014-08-17 | E-GEOD-45512 | biostudies-arrayexpress

Mus musculus

Project description:Illumina array to compare whole-genome expression change in miR-127 KO mice at E18.5 in 3 tissues: brain, skin and muscle

| PRJNA203647 | ENA

Mutual regulation of miR-22 and ERalpha in muscle tissue

Project description:Expression profiling of muscle tissue isolated from WT, miR-22 KO, miR-22/ERalpha KO, and miR-22KO/muscle specific ERalphaKO

2017-03-13 | E-MTAB-3518 | biostudies-arrayexpress

miR-127-3p is an epigenetic activator of myofibroblast senescence situated within the miRNA enriched Dlk1-Dio3 imprinted domain on mouse chromosome 12 [miRNA array]

Project description:During wound healing, fibroblasts differentiate into non-proliferative contractile myofibroblasts, contribute to skin repair, and eventually undergo apoptosis or become senescent. MicroRNAs (miR) are posttranscriptional regulators of gene expression networks that control cell fate and survival and may also regulate senescence. Here we determined regulated miRs in myofibroblasts isolated from wounds and analyzed their role in senescent myofibroblast formation. Transcriptome profiling showed that a 200 kbp region of the Dlk1-Dio3 imprinted domain on mouse chromosome 12 encodes for most of the upregulated miRs in the entire genome of mouse myofibroblasts. Among those, miR-127-3p induced a myofibroblast-like phenotype associated with a block in proliferation. Molecular analysis revealed that miR-127-3p induced a prolonged cell-cycle arrest with unique molecular features of senescence, including the activation of the senescence-associated ß-galactosidase, increase in p21 levels, inhibition of lamin B1, proliferation factors, and the production of senescence-associated inflammatory and extracellular matrix -remodeling components. Hence, miR-127-3p emerges as an epigenetic activator regulating the transition from repair to remodeling during skin wound healing, but may also induce age-related defects, pathological scarring and fibrosis, all linked to myofibroblast senescence.

2021-01-31 | GSE160921 | GEO

miR-127-3p is an epigenetic activator of myofibroblast senescence situated within the miRNA enriched Dlk1-Dio3 imprinted domain on mouse chromosome 12 [mRNA array]

2021-01-31 | GSE160920 | GEO

MiRNA-127 Inhibits IgG Immune Complex-induced Lung Inflammation by Targeting IgG Fcγ Receptor I

Project description:The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. MiR-127 appeared to be down-regulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of the regulation of inflammation by miR-127, we found that IgG Fcγ Receptor I (FcγRI/CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages over-expressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3’-UTR of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex (IgG IC) model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or non-infectious lung injury.

2012-04-04 | GSE27642 | GEO

microRNA-1 Regulates Metabolic Flexibility in Skeletal Muscle via Pyruvate Metabolism

Project description:MicroRNA-1 (miR-1) is the most abundant miRNA in adult skeletal muscle. To determine the function of miR-1 in adult skeletal muscle, we generated an inducible, skeletal muscle-specific miR-1 knockout (KO) mouse. Integration of RNA-sequencing (RNA-seq) data from miR-1 KO muscle with Argonaute 2 enhanced crosslinking and immunoprecipitation sequencing (AGO2 eCLIP-seq) from human skeletal muscle identified miR-1 target genes involved with glycolysis and pyruvate metabolism. The loss of miR-1 in skeletal muscle induced cancer-like metabolic reprogramming, as shown by higher pyruvate kinase muscle isozyme M2 (PKM2) protein levels, which promoted glycolysis. Comprehensive bioenergetic and metabolic phenotyping combined with skeletal muscle proteomics and metabolomics further demonstrated that miR-1 KO induced metabolic inflexibility as a result of pyruvate oxidation resistance. While the genetic loss of miR-1 reduced endurance exercise performance in mice and in C. elegans, the physiological down-regulation of miR-1 expression in response to a hypertrophic stimulus in both humans and mice may cause a similar metabolic reprogramming that supports muscle cell growth. Taken together, these data identify a novel post-translational mechanism of adult skeletal muscle metabolism regulation mediated by miR-1.

2024-08-09 | GSE274378 | GEO

Expression data from miR-205 knockout in Hair Follicle Stem Cells (HFSCs) of mouse skin

Project description:We identified 201 genes that are consistently upregulated more than 20%, and 108 genes that are consistently downregulated more than 20% in the miR-205 KO samples in two sets of biological duplicates. We used microarrays to measure transcriptome changes upon knockout of miR-205 in hair follicle stem cells of mouse skin and identified new targets of miR-205. We isolated the HFSCs from WT and miR-205 KO skin at P4 and compare mRNA expression by microarray analysis

2013-08-20 | E-GEOD-46447 | biostudies-arrayexpress

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