Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA203647 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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. 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.
2014-05-20 | E-GEOD-47110 | biostudies-arrayexpress
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
Project description:Purpose: The goal of this study is to compare the cardiac transcriptome profiling (RNA-seq) of WT and CHD4-M195I hearts at E18.5 to conclude genes affected by this CHD4 mutation. Methods: mRNA profiles of E18.5 WT and CHD4-M195I mouse hearts were generated by deep sequencing, n=4 for each genotype, using Illumina HiSeq2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: RNA-sequencing (RNA-seq) analyses on E18.5 WT and CHD4-M195I hearts and identified 323 genes that were differentially expressed [adjusted P value <0.05, |log2(Fold Change)| > 0.5], 113 upregulated and 210 downregulated in CHD4-M195I hearts.
2023-05-08 | GSE229050 | GEO
Project description:We profiled the expression of circulating microRNAs (miRNAs) in mice exposed to gram-positive and gram-negative bacteria using Illumina small RNA deep sequencing. Recombinant-specific gram-negative pathogen Escherichia coli (Xen14) and gram-positive pathogen Staphylococcus aureus (Xen29) were used to induce bacterial infection in mice at a concentration of 1 × 108 bacteria/100 μL of phosphate buffered saline (PBS). Small RNA libraries generated from the serum of mice after exposure to PBS, Xen14, Xen29, and Xen14+Xen29 via the routes of subcutaneous injection (I), cut wound (C), or under grafted skin (S) were analyzed using an Illumina HiSeq2000 Sequencer. Following exposure to gram-negative bacteria alone, no differentially expressed miRNA was found in the injection, cut, or skin graft models. Exposure to mixed bacteria induced a similar expression pattern of the circulating miRNAs to that induced by gram-positive bacterial infection. Upon gram-positive bacterial infection, 9 miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133a-1-5p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p, mir-215-5p) showed upregulation greater than 4-fold with a p-value < 0.01. Among them, mir-193b-3p, mir-133a-1-3p, and mir-133a-2-3p presented the most common miRNA targets expressed in the mice exposed to gram-positive bacterial infection.
2014-08-19 | GSE60492 | GEO
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 | GSE160920 | GEO
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
Project description:This array is designed to compare the differentially expressed genes in control mouse skin and keratinocytes-specific N-WASP knockout mouse skin (k5 cre). Ext-01 file is the array analysis from backskin of control mouse and Ext-02 file is the array analysis from backskin of N-WASP ko mouse.
2018-03-06 | E-MTAB-6580 | biostudies-arrayexpress
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
Project description:Single cell sequence (SC-seq) has been used to explore the effect of miR-21-modulated chemotherapy-induced tumor microenvironment change. MTC-Q1 WT or MTC-Q1 miR-21 KO cells were subcutaneously injected into C57BL/6 mice. CD45+ immune cells has been isolated after cisplatin injection. The isolated immune cell were sequenced by dropped based scRNA-seq, cDNA were sequenced by Illumina Novaseq 6000.
2022-08-29 | GSE172326 | GEO