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Aurothioglucose Enhances Pro-Angiogenic Pathway Activation in Lungs from Room Air and Hyperoxia-exposed Newborn Mice

ABSTRACT: Aurothioglucose Enhances Pro-Angiogenic Pathway Activation in Lungs from Room Air and Hyperoxia-exposed Newborn Mice

PROVIDER: PRJNA608719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11179940_1.fastq.gz	Fastqsanger.gz
	SRR11179940_2.fastq.gz	Fastqsanger.gz
	SRR11179941_1.fastq.gz	Fastqsanger.gz
	SRR11179941_2.fastq.gz	Fastqsanger.gz
	SRR11179942_1.fastq.gz	Fastqsanger.gz

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Aurothioglucose Enhances Pro-Angiogenic Pathway Activation in Lungs from Room Air and Hyperoxia-exposed Newborn Mice

Project description:Acute neonatal muring hyperoxia exposure to evaluate the impact of the TXNRD1 inhibitor aurothioglucose on pulmonary response and gene expression.

2020-07-15 | GSE145912 | 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

Microarray data of the subventricular zone and hippocampal tissue from mice exposed to room air or hyperoxia during the neonatal period

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

Expression data from 8-10 week old WT mice maintained in room air or exposed to hyperoxia (FiO2>95%) for 48 hrs

2014-12-10 | GSE51039 | GEO

Se Deficiency Exacerbates Hyperoxia-Induced Lung Injury in Newborn C3H/HeN Mice

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

Aurothioglucose enhances proangiogenic pathway activation in lungs from room air and hyperoxia-exposed newborn mice.

Project description:Bronchopulmonary dysplasia (BPD), a long-term respiratory morbidity of prematurity, is characterized by attenuated alveolar and vascular development. Supplemental oxygen and immature antioxidant defenses contribute to BPD development. Our group identified thioredoxin reductase-1 (TXNRD1) as a therapeutic target to prevent BPD. The present studies evaluated the impact of the TXNRD1 inhibitor aurothioglucose (ATG) on pulmonary responses and gene expression in newborn C57BL/6 pups treated with saline or ATG (25 mg/kg ip) within 12 h of birth and exposed to room air (21% O2) or hyperoxia (>95% O2) for 72 h. Purified RNA from lung tissues was sequenced, and differential expression was evaluated. Hyperoxic exposure altered ~2,000 genes, including pathways involved in glutathione metabolism, intrinsic apoptosis signaling, and cell cycle regulation. The isolated effect of ATG treatment was limited primarily to genes that regulate angiogenesis and vascularization. In separate studies, pups were treated as described above and returned to room air until 14 days. Vascular density analyses were performed, and ANOVA indicated an independent effect of hyperoxia on vascular density and alveolar architecture at 14 days. Consistent with RNA-seq analyses, ATG significantly increased vascular density in room air, but not in hyperoxia-exposed pups. These findings provide insights into the mechanisms by which TXNRD1 inhibitors may enhance lung development.

| S-EPMC7347274 | biostudies-literature

Expression data from 8-10 week old WT mice maintained in room air or exposed to hyperoxia (FiO2>95%) for 48 hrs

Project description:To detect sex-specific differences in gene expression in a model of hyperoxic lung injury in adult C56BL/6J mice. In this dataset, we include the expression data obtained from lungs from 8-10 week old male and female WT C57BL/6J mice exposed to hyperoxia for 48 hours amd room air controls.These data were used to determine differences in transcriptome between male and female mice after hyperoxia exposure 12 total samples were analyzed. We generated the following pairwise comparisons: 5 comparisons (M/F: male/female, A/O: air/oxygen): 1) M_O - M_A,  2) F_O - F_A, 3) M_O - F_O, 4) M_A - F_A, 5) (M_O - M_A) - (F_O - F_A). Genes with an FDR≤5% and a fold-change ≥1.4 were selected.

2014-12-10 | E-GEOD-51039 | biostudies-arrayexpress

Effect of GSDMD knockout on hyperoxia-induced lung and retinal injury

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

Se Deficiency Exacerbates Hyperoxia-Induced Lung Injury in Newborn C3H/HeN Mice

Project description:Se Deficiency Exacerbates Hyperoxia-Induced Lung Injury in Newborn C3H/HeN Mice

| PRJNA1076259 | ENA

Affymetrix analysis of adult mouse lung exposed to room air or 100% oxygen between postnatal days 0-4

Project description:It is unclear why preterm birth increases risk of cardiovascular disease later in life. Studies in mice indicate excess oxygen 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. Here, affymetrix gene arrays were used to identify early transcriptional changes in lungs of young adult mice exposed to room air or 100% oxygen between postnatal days 0-4.

2018-01-01 | E-MTAB-6074 | biostudies-arrayexpress

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