Neonatal mouse exposed to hyperoxia
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ABSTRACT:
PROVIDER: PRJNA531182 | ENA |
REPOSITORIES: ENA
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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:Premature infants often require oxygen therapy, which increases the risk of bronchopulmonary dysplasia and long-term cognitive impairment. The prefrontal cortex (PFC), essential for higher-order cognition, may be particularly vulnerable to neonatal hyperoxia, yet the cellular and molecular effects remain unclear. We exposed C57Bl/6 mouse pups to hyperoxia (85% O₂) or normoxia from postnatal days 1–14 and performed single nucleus RNA and ATAC sequencing of the PFC, complemented by oligodendrocyte progenitor cell assays and validation in mouse and human brain tissues. Hyperoxia reduced L4/5 intratelencephalic projecting glutamatergic neurons in females and mature oligodendrocytes in males, accompanied by consistent repression of myelination genes proteolipid protein 1 (Plp1) and myelin basic protein (Mbp) and altered chromatin accessibility. Oligodendrocyte transcription factor 2 (Olig2) was induced in both sexes, whereas lysine demethylase 3A (Kdm3a) activation was female specific. Hyperoxia activated Netrin-1 signaling in males and disrupted tumor protein p53 (TP53)-regulated metabolic pathways in females. Oligodendrocyte progenitor cell proliferation and differentiation were inhibited in vitro, and human bronchopulmonary dysplasia PFC samples recapitulated these core alterations. Together, these findings demonstrate that neonatal hyperoxia disrupts PFC development through sex-dependent effects on neuronal differentiation, oligodendrocyte maturation, and transcriptional regulation. Concordant mouse-human myelination deficits highlight the pathological relevance of oxygen exposure and underscore the importance of considering sex as a biological variable in preterm brain injury.
2026-07-15 | GSE331357 | GEO
Project description:This experiment aimed to investigate the differences in the transcriptional profile of the neurogenic niche regions of mouse pups that were raised in room air verses mouse pups that were exposed to hyperoxia during the neonatal period. Pups were housed in room air or hyperoxia (85% O2) from P0 to P14. Brain tissue (the subventricular zone and the hippocampus) was collected at P14 and 12 months of age. RNA was extracted from the brain tissue and the microarray labelling, hybridization, and scanning was conducted by the Génome Québec Innovation Centre (Montréal, Canada).
2023-01-03 | E-MTAB-11332 | biostudies-arrayexpress
Project description:miR-30a -/- neonatal mice were exposed to hyperoxia [95% FiO2, postnatal day (PND) 1-5] or room air before being euthanized on PND 21.
2025-09-12 | GSE213287 | 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:We evaluated the transcriptional changes in the aorta and kidney of 1 year old rats that were exposed to hyperoxia or normoxia in the neonatal period.
2024-06-30 | GSE234635 | GEO
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: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:Global gene expression changes in the lung and ileum of hyperoxia-exposed neonatal mice
| PRJNA516566 | ENA
Project description:Exposure to neonatal hyperoxia is associated with brain injury and poor neurodevelopmental outcomes in preterm infants. Our goal was to determine the pathogenic role of GDMD in hiipocampal in injury in newborn mice
2023-09-13 | GSE241549 | GEO