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Effect of glutathione reductase (Gsr) deficiency on lung transcriptomics in embryonic mice and neonatal and adult mice exposed to hyperoxia.

ABSTRACT: Effect of glutathione reductase (Gsr) deficiency on lung transcriptomics in embryonic mice and neonatal and adult mice exposed to hyperoxia.

PROVIDER: PRJNA478826 | ENA |

REPOSITORIES: ENA

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Effect of glutathione reductase (Gsr) deficiency on lung transcriptomics in embryonic mice and neonatal and adult mice exposed to hyperoxia.

Project description:Gsr is an antioxidant enzyme responsible for maintaining the supply of reduced glutathiones which reduce reactive oxigen species and maintain cellular redox balance. However, the the role for Gsr in the developemnt of oxidative lung injury is not well characterized. We used microarray analysis to identify Gsr-dependent genes and pathways in embyronic, neonate, and adult lungs. We also determined Gsr-dependent lung transcriptomics in mouse neonates and adults which were neonatally exposed to hyperoxia (O2) or air.

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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.

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RNA-sequencing analysis reveals mitochondrial dysfunction in Akap1 Knockout mice exposed to hyperoxia

Project description:Akap1 KO and Wt mice were exposed to normoxia or hyperoxia for 48h. Total RNA was extracted from lungs of Wt Normoxia (n=3), Wt hyperoxia (n=3), Akap1 KO (n=3) and Akap1 hyperoxia (n=3) mice. RNA-sequencing was carried out followed by differential expression of genes in the following groups. Wt Normoxia vs Wt Hyperoxia, Akap1 KO Normoxia versus Akap1 KO Hyperoxia, Wt Normoxia versus Akap1 KO Normoxia and Wt Hperoxia versus Akap1 Hyperoxia.

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Interactions between H2O2 and glutathione in gene expression

Project description:rs08-03_glutathion - glutathion - How does glutathione content or reduction state affect H2O2-induced changes in the transcriptome? - Three single Arabidopsis mutants were used: cat2, knockout for catalase2 and so enriched in H2O2; cad2, defective in glutathione content; cytGR, knockout for cytosolic glutathione reductase. Cat2 was crossed with cad2 and cyt GR, and col0, 3 single mutants, and 2 double mutants were sampled in controlled growth conditions either in 8h or 16h photoperiod. Keywords: gene knock out 20 dye-swap pairs - CATMA arrays: 40 arrays

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