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Mus musculus

ABSTRACT: Whole-transcriptome profiling of neovascularized corneas reveal miR-204 as a potent biotherapy deliverable by rAAVs [RNA-Seq]

PROVIDER: PRJNA352487 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4926510_1.fastq.gz	Fastqsanger.gz
	SRR4926510_2.fastq.gz	Fastqsanger.gz
	SRR4926511_1.fastq.gz	Fastqsanger.gz
	SRR4926511_2.fastq.gz	Fastqsanger.gz
	SRR4926512_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Mus musculus

Project description:Whole-transcriptome profiling of neovascularized corneas reveal miR-204 as a potent biotherapy deliverable by rAAVs [nCounter - microRNAs]

| PRJNA352486 | ENA

Whole-transcriptome profiling of neovascularized corneas reveal miR-204 as a potent biotherapy deliverable by rAAVs

Project description:Whole-transcriptome profiling of neovascularized corneas reveal miR-204 as a potent biotherapy deliverable by rAAVs

| PRJNA352483 | ENA

Whole-transcriptome profiling of neovascularized corneas reveal miR-204 as a potent biotherapy deliverable by rAAVs [nCounter - microRNAs]

Project description:Current drugs that directly target pro-angiogenic factors to inhibit or reverse corneal neovascularization, the major sight-threatening pathology caused by angiogenic stimuli, require multiple rounds of administration and have limited efficacies. Here we report the profiling of anti-angiogenic corneal microRNAs (miRNAs), and a framework that employs discovered miRNAs as biotherapies deliverable by recombinant adeno-associated viruses (rAAVs). By querying differentially expressed miRNAs in neovascularized mouse corneas induced by alkali-burn, we have revealed 39 miRNAs that are predicted to target more than 5,500 differentially expressed corneal mRNAs. Among these corneal miRNAs, we selected miR-204 and assessed its efficacy as a therapeutic miRNA in injured corneas. Our results show that delivery of miR-204 by rAAV is efficacious and safe for mitigating corneal NV. Overall, our work demonstrates the discovery of therapeutic miRNAs in corneal disorders and their translation into viable clinical vectors.

2018-10-26 | GSE89536 | GEO

Whole-transcriptome profiling of neovascularized corneas reveal miR-204 as a potent biotherapy deliverable by rAAVs [RNA-Seq]

2018-10-26 | GSE89537 | GEO

Expression profile of HCT116 cells transfected with miR-204-5p

Project description:We have employed whole genome microarray expression profiling as a discovery platform to screen potential target genes of miR-204-5p in colorectal cancer cell HCT116. HCT116 cells were seeded in 6-cm2 tissue culture plates and transfected with the miR-204-5p mimic or negative control (NC) using Lipofectamine 2000 (Invitrogen, USA). After propagation for 48 hours, total RNA was extracted using TRIzol reagent (Invitrogen, USA). Expression profiling was performed using an Agilent human whole genome oligo microarray chip (4M-CM-^W44K) (Agilent, USA) Expression profiling in HCT116 cells was measured at 48 hours after transfection with miR-204-5p or negative control. Experiments were performed using the two samples without repeat experiment.

2014-07-30 | E-GEOD-59897 | biostudies-arrayexpress

Expression profile of HCT116 cells transfected with miR-204-5p

2014-07-30 | GSE59897 | GEO

RNA-seq of miR-204-5p overexpressing 4T1 murine breast cancer cells

Project description:We established two distinct stable clones which ectopically overexpress miR-204-5p to different levels, then performed transcriptome profiling of miR-204-5p overexpressing cells compared to control 4T1 cells to understand the molecular mechanisms of the miR-204-5p’s effect on cancer cells.

2021-01-26 | GSE109725 | GEO

MIR-204 target genes

Project description:The aim of this study is to discover genes regulated by miR-204. Differential gene expression in HEK-293 cells transfected with miR-204-mimic compared to HEK-293 cells transfected with control oligo (HEK-293 control) was analyzed using the Agilent Human Whole Genome 4x44K gene expression array (Agilent Technologies, Santa Clara, CA). HEK-293 cells were transfected with either miR-204 or a control, and gene expression was analyzed using the Agilent Human Whole Genome 4x44K array. A dye-swap was performed.

2012-03-30 | E-GEOD-28400 | biostudies-arrayexpress

MIR-204 target genes

2012-03-31 | GSE28400 | GEO

Exercise promotes peripheral glycolysis through miR-204 induction in skeletal muscle

Project description:Mechanisms underlying exercise induced insulin sensitization are of interest as exercise is a clinically critical option as a lifestyle intervention for diabetic patients. Some of microRNAs (miRNAs), which can be secreted from skeletal muscle after exercise, regulate insulin sensitivity and are used for diagnostic marker for diabetic patients. MiR-204 is well-known for its involvement in development, cancer, and metabolism. However, it is still unknown whether miR-204 associates with exerciseinduced glycemic control. In preliminary data, we found that endurance exercise of mice increases miR-204 expression levels in skeletal muscle. In chronic exercise mice model, miR-204 expression levels were increased with glycolytic enzymes in skeletal muscle. When hypoxia induced hypoxia inducible factor 1 alpha (HIF1α), miR-204 expression levels were increased. HIF1α overexpression also increased miR-204 expression levels. To corroborate the causality between miR-204 and glycolysis, miR-204 mimic was introduced to myoblast cell line, C2C12 myoblast cell line. After exposure to miR-204 mimic, C2C12 cells could increase the glycolysis rate measured by extracellular acidification rate. miR-204 mimics also increased mRNA expression levels of glycolytic enzymes. In vivo intravenous miR-204 administration to mice also increased the glucose clearance rate after refeeding of mice. MiR-204 increased blood glucose surge on earlier point of refeeding but promoted the blood glucose lowering on later point of refeeding. Skeletal muscle glycolytic enzymes were increased in mRNA expression levels by miR-204 injection. This finding suggests the novel physiological role of miR-204 in skeletal muscle glycolysis where insulin action is limited.

2024-09-04 | GSE276372 | GEO

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