Transcriptomic profiling of the preterm,hyperoxia exposed, rabbit's lung
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ABSTRACT:
PROVIDER: PRJNA1198981 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31737101_1.fastq.gz | Fastqsanger.gz | |||
| SRR31737101_2.fastq.gz | Fastqsanger.gz | |||
| SRR31737102_1.fastq.gz | Fastqsanger.gz | |||
| SRR31737102_2.fastq.gz | Fastqsanger.gz | |||
| SRR31737103_1.fastq.gz | Fastqsanger.gz |
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Project description:Bronchopulmonary dysplasia (BPD) is a multifactorial chronic lung disease of premature neonates. The development of BPD depends on several prenatal and postnatal factors that induce inflammation, altering alveolar growth and pulmonary vascular development. Animal models are essential to investigating the precise molecular pathways leading to BPD. The preterm rabbit combines many advantages of both small (e.g., rodents) and large BPD models (i.e., preterm lambs and baboons). For instance, preterm rabbits display mild-to-moderate respiratory distress at delivery, which, along with ongoing exposure to high oxygen concentration (95% O2), leads to functional and morphological lung changes that resemble the phenotype of human BPD. Nevertheless, the molecular pathways leading to the development of the BPD-like phenotype in this model remain largely ununderstood. We, therefore, aimed to characterize the longitudinal gene expression in the lungs of preterm rabbits continuously exposed to 95% O2 on postnatal days 3, 5, and 7. The longitudinal transcriptomic analysis revealed different expression patterns for several genes and pathways. Over time, extracellular matrix organization and angiogenesis were increasingly downregulated, while apoptosis, RNA processing, and inflammation showed the opposite trend.
2025-04-14 | GSE284417 | GEO
Project description:Extremely preterm infants are often treated with supraphysiological oxygen which contributes to the development of bronchopulmonary dysplasia (BPD). These same infants exhibit compromised antioxidant capacities due in part to selenium (Se) deficiency. The present study was designed to develop a perinatal Se deficiency mouse model, identify the effects of newborn hyperoxia exposure, and explore alternative pathways affected by Se deficiency (SeD) that would contribute to impaired lung development. Se deficient breeding pairs were generated, once pups were born, they were exposed to room air or 85% O2 for 14 d. Survival, antioxidant and Nrf2-regulated protein expression, and RNA seq analyses were performed. Greater than 40% mortality was observed in Se deficient (SeD), hyperoxia exposed pups. Surviving SeD pups had greater lung growth deficits than Se sufficient (SeS) pups exposed to hyperoxia. Gpx2 and 4 protein and Gpx activity were significantly decreased in SeD pups. Nrf2-regulated proteins, NQO1 and Gclc were increased in the setting of Se deficiency and hyperoxia exposure. RNA seq revealed significant decreases in the Wnt/-catenin and Notch pathways. Se is a biologically relevant modulator of perinatal lung development and antioxidant responses, especially in the context of hyperoxia exposure. RNA seq implicates pathways essential for normal lung development are dysregulated by Se deficiency.
2024-05-01 | GSE255744 | GEO
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
Project description:To investigate the role of GSDMD-mediated pyroptosis in neonatal lung and retinal injury induced by hyperoxia We performed RNA-seq of lung and retina of newborn rats exposed to hyperoxia for 2 weeks
2023-01-11 | GSE206087 | GEO
Project description:Background: Bronchopulmonary dysplasia (BPD), the most common complication of extreme preterm birth, can be caused by oxygen-related lung injury and is characterized by impaired alveolar and vascular development. Mesenchymal stromal cells (MSCs) have lung protective effects. Conversely, BPD is associated with increased MSCs in tracheal aspirates. Objective: To determine whether endogenous lung (L-)MSCs are perturbed in a well-established oxygen-induced rat model mimicking BPD features. Methods: Rat pups were exposed to room air or 95% oxygen from birth to postnatal day 10. On day 12, CD146+ L-MSCs were isolated and characterized according to the International Society for Cellular Therapy criteria. Epithelial and vascular repair potential were tested by scratch assay and endothelial network formation respectively, immune function by mixed lymphocyte reaction assay. Microarray analysis was performed using the Affymetrix GeneChip and gene set enrichment analysis (GSEA) software. Results: CD146+ L-MSCs isolated from rat pups exposed to hyperoxia had decreased CD73 expression and inhibited lung endothelial network formation. CD146+ L-MSCs indiscriminately promoted epithelial wound healing and limited T-cell proliferation. Expression of potent anti-angiogenic genes of the axonal guidance cue and CDC42 pathways was increased after in vivo hyperoxia, whereas genes of the anti-inflammatory JAK/STAT and lung/vascular growth promoting Fibroblast Growth Factor (FGF) pathways were decreased. Conclusions: In vivo hyperoxia exposure alters the pro-angiogenic effects and FGF expression of L-MSCs. Additionally, decreased CD73 and JAK/STAT expression suggest decreased immune function. L-MSC function may be perturbed and contribute to BPD pathogenesis. These findings may lead to improvements in manufacturing exogenous MSCs with superior repair capabilities.
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Project description:Neonatal mouse exposed to hyperoxia
| PRJNA531182 | ENA
Project description:Preterm infants exposed to supplemental oxygen (hyperoxia) are at risk for developing heart failure later in life. Rodent studies show that exposure to hyperoxia in early postnatal life causes heart failure later in life that resembles heart failure in humans who were born preterm. Neonatal hyperoxia exposure affected the left atrium and left ventricle differently, inhibiting the proliferation and survival of atrial cardiomyocytes while enhancing cardiomyocyte differentiation in the ventricle. In this study, whole genome transcriptomics revealed the left atria of neonatal mice are more responsive to hyperoxia than the left ventricle, with the expression of 4,285 genes affected in the atrium and 1,743 in the ventricle. While hyperoxia activated p53 target genes in both chambers, it caused greater DNA damage, phosphorylation of the DNA damage responsive ataxia telangiectasia mutated (ATM) kinase, mitochondrial stress, and apoptosis in the atrium. In contrast, hyperoxia induced the expression of DNA repair and growth arrest genes in the ventricle. Atrial cells also showed a greater loss of extracellular matrix and superoxide dismutase 3 (SOD3) expression, possibly contributing to the enlargement of the left atrium and reduced velocity of blood flow across the mitral valve seen in hyperoxia exposed mice. Diastolic dysfunction and heart failure in hyperoxia exposed mice may thus stem from its effects on the left atrium, suggesting chamber-specific therapies may be needed to address diastolic dysfunction and heart failure in people who were born preterm.
2025-02-25 | GSE282365 | GEO
Project description:We performed miRNA array analysis from 2 groups (neonatal lung control, neonatal lung after hyperoxia). We used pools of every 100ng of total RNA of three samples for each groups.
2021-04-06 | GSE129406 | GEO
Project description:To investigate the effects of ATRA on hyperoxia-induced inflammatory responses in A549 lung adenocarcinoma cells, we exposed A549 cells (both ATRA- and control-treated) to hyperoxia. We then performed gene expression profiling analysis using data obtained by RNA-seq.
2022-05-11 | GSE202458 | GEO
Project description:Ths study addressed the hypothesis that exposure to hyperoxia alters gene expression in both the lung and the ileum, but that the gene epxression cahnges are specific to each organ. The data indicat ethat there are highly specific changes in each organ due to hyperoxia.
2019-01-24 | GSE125489 | GEO