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Expression profiles of mRNAs in the retinas of OIR wildtype, OIR IL-19 knockout and room air control mice.

ABSTRACT: Expression profiles of mRNAs in the retinas of OIR wildtype, OIR IL-19 knockout and room air control mice.

PROVIDER: PRJNA799358 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17695688_1.fastq.gz	Fastqsanger.gz
	SRR17695688_2.fastq.gz	Fastqsanger.gz
	SRR17695689_1.fastq.gz	Fastqsanger.gz
	SRR17695689_2.fastq.gz	Fastqsanger.gz
	SRR17695690_1.fastq.gz	Fastqsanger.gz

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Expression profiles of mRNAs in the retinas of OIR wildtype, OIR IL-19 knockout and room air control mice.

Project description:Seven-day-old C57BL/6 mice and IL-19 knockout (KO) mice were subjected to 75% oxygen for 5 days to induce OIR. To explore the mechanism that caused by IL-19 on retinal neovascularization, Gene expressions among retinas of room air control mice, OIR wildtype mice, and OIR IL-19 knockout mice were measured by RNA-sequencing (RNA-seq).

2022-01-24 | GSE194176 | GEO

Expression profiling of microRNAs in oxygen-induced retinal neovascularization in mice

Project description:The purpose of this study is to identify disease-related miRNAs in retinas of a mouse model of oxygen-induced retinopathy (OIR). OIR pups were exposed to 75% oxygen at postnatal day (P)7 for 5 days, and were returned to room air at P12. The miRNAs expression profiles in the retinas from OIR mice at P17 and room air controls were determined through microarray analysis. Expressions of significantly upregulated and downregulated miRNAs in the OIR retinas and controls were confirmed through quantitative real-time RT-PCR (qPCR). Compared to the room air controls, 3 miRNAs were significantly up-regulated, and 8 miRNAs were down-regulated in OIR retinas. Our findings indicated that several miRNAs were differentially expressed in the oxygen-induced retinal neovascularization, which might provide novel therapeutic targets in regulating retinal neovascular diseases.

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Gene expression microarray analysis of early oxygen-induced retinopathy (OIR)

Project description:Different inbred strains of rats differ in their susceptibility to OIR, an animal model of human retinopathy of prematurity. We examined gene expression profiles in Fischer 344 (F344, resistant to OIR) and Sprague Dawley (SD, susceptible to OIR) rats at the early time point of day 3 to identifying gene pathways related to the underlying genetic cause of phenotypic differences between strains. To examine gene expression changes in rats strains which are resistant and susceptible to OIR, four different experimental conditions were analysed: F344 cyclic hyperoxia (O2) exposed, F344 room air (RA) exposed, SD O2 exposed and SD RA exposed. A minimum of two samples of pooled RNA, comprising of 3 individual rats from 2 separate litters, was used for each experimental condition. Pooled RNA from different rats were used as biological replicates. An additional sample for F344 O2 and SD RA rats was included on the basis of the principal components analysis from the initial 8 samples. Pooled RNA from age-matched room air-exposed rats were used as controls.

2009-11-12 | E-GEOD-18998 | biostudies-arrayexpress

Profiling the retinal microRNA (miRNA) transcriptomes in a rat model of oxygen-induced retinopathy (OIR) by next-generation sequencing

Project description:Purpose: The study aimed to determine the transcriptome profile of retinal miRNA in a Sprague Dawley (SD) rat model of oxygen-induced retinopathy Methods: The newborn rats in OIR group were subjected to daily cycles of 80% oxygen for 21 hours and room air for 3 hours in a customised chamber for 14 days (postnatal day 14, P14), then return to room air for 15 days (postnatal day 29, P29). The newborn rats in sham group were housed in room air for 14 days. Retinal miRNA expression profiles of OIR or sham rats at P14 or OIR rats at P29 were generated by deep sequencing, in triplicate, using Illumina Hiseq-2500 RNA-seq platform. Briefly, the sequence reads from all samples were analysed for overall quality, screened for the presence of any contaminants and trimmed accordingly. The cleaned sequence reads were then processed through the quantification modules miRDEEP2 ver2.0.0.7 pipeline for known miRNA expression profiling. Rat miRNAs from miRBASE release21 were used for mapping and quantification. Differential miRNA expression analysis was undertaken using voom bioconductor package (https://www.bioconductor.org/packages/release/bioc/vignettes/limma/inst/doc/usersguide.pdf). Results: A total of 465 miRNAs were identified in the rat retina. The miRNAs with significantly altered levels (P<0.05) were identified in OIR rats at P14 compared with the sham controls or OIR rats at P29. Among those altered miRNAs, seven miRNAs were down-regulated in OIR rats at P14 with Log2 (Fold Change) < -1 fold, and no miRNAs were up-regulated. Additionally, the expression of these down-regulated miRNAs in OIR rats at P14 was restored at P29 after they were exposed to room air. Conclusion: Our study represents the first detailed analysis of retinal miRNA expression profile in rat model of OIR by miRNA-NGS technology.

2022-10-01 | GSE104620 | GEO

Use of microarray analyses to determine the effect of hyperoxia and hypoxia on gene expression in early oxygen-induced retinopathy (OIR).

Project description:Different inbred strains of rats differ in their susceptibility to OIR, an animal model of human retinopathy of prematurity. We examined gene expression profiles in Fischer 344 (F344, resistant to OIR) and Sprague Dawley (SD, susceptible to OIR) rats at the early time points of day 5 (in response to hyperoxia) and day 6 (in response to relative hypoxia) to identify gene pathways related to the underlying genetic cause of the phenotypic differences observed between strains. To examine gene expression changes in rat strains which are resistant and susceptible to OIR, four different experimental conditions were analysed: F344 cyclic hyperoxia (O2) exposed, F344 room air (RA) exposed, SD O2 exposed and SD RA exposed. Two samples of pooled RNA, comprising of 3 individual rats from 2 separate litters, was used for each experimental condition, for each time point of interest. Pooled RNA from age-matched room air-exposed rats were used as controls.

2012-02-24 | E-GEOD-36037 | biostudies-arrayexpress

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RNA-sequencing of the oxygen induced retinopathy (OIR) model in C57BL/6 mice

Project description:Pathological retinal angiogenesis is one of the major causes of vision loss worldwide. The breakdown of blood vessels and aberrant vessels growth usually lead to hemorrhage, macular edema, fibrotic scar, and retinal detachment. OIR model serves as a proxy for human pathological retinal neovascularization such as proliferative diabetic retinopathy, retinal vein occlusion and retinopathy of prematurity. C57BL/6 mice were exposed to 75% O2 in a hyperoxic chamber from postnatal day P7 to P12 and then returned to room air. The greatest neovascular response occurred at postnatal 17 days (P17) when the mice are put back to room air condition for 5 days. In order to reveal potential genes that involve in pathological neovascularization, we performed transcriptomic analyses of retina of P17.

2024-08-20 | GSE241239 | GEO

Hippocamppal gene expression - C57BL/6 mice exposed to room air or 85% oxygen from P2-P14

Project description:We are reporting the RNA sequence of hippocamppal samples obtained from C57BL/6 mice at P14 following room air or 85% exposure from P2-14

2018-12-14 | GSE111189 | GEO

Profiles of N6-methyladenosine modifications of circular RNAs in oxygen-induced retinopathy

Project description:To identify the N6-methyladenosine (m6A) modified circular RNAs (circRNAs) involved in a mouse model of oxygen-induced retinopathy (OIR), microarray analysis was performed with the retinal samples from OIR mice and Room air controls.

2023-01-31 | GSE213362 | GEO

Affymetrix array of postnatal day 4 mouse atria exposed to room air or hyperoxia

Project description:It is unclear why preterm birth increases risk of cardiovascular disease later in life. Studies in mice indicate excess oxygen typically used to treat preterm infants causes pulmonary hypertension, cardiac failure, and shortens lifespan. We previously reported neonatal hyperoxia causes pulmonary hypertension in aged mice as defined pathologically by pulmonary capillary rarefaction, dilation of pulmonary arterioles and veins, right ventricular hypertrophy, and reduced lifespan. These changes were preceded by a pronounced growth inhibition of cardiomyocytes lining the pulmonary vein and extending into the left atria, resulting in diastolic heart failure as the mice aged. To identify transcriptional changes by which hyperoxia suppresses proliferation of these cardiomyocytes, newborn mice were exposed to room air or 100% oxygen between birth and postnatal day 4. RNA was then isolated from atria of 3 room air and 4 hyperoxia-exposed mice and used to probe Affymetrix mouse array 430 versus 2.0

2021-02-23 | E-MTAB-9008 | biostudies-arrayexpress

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