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- W2898771888 abstract "Bronchopulmonary Dysplasia (BPD) is a chronic lung disease that affects pre-term infants whose lungs are unable to support life outside of the womb. These babies receive therapeutic oxygen which compensates for poor lung function but also causes oxidative damage to lung epithelium, resulting in a simplified lung marked by larger and fewer alveoli. We identified thioredoxin-1 (Trx1) as a protein of interest in the pathogenesis of BPD since Trx1 is cytoprotective against hyperoxic cell death. Using a perinatal hyperoxic mouse model of BPD, pulmonary Trx1 activity inversely correlates with atmospheric oxygen tension following birth and hyperoxic treatment. Therefore, we tested if impairment of lung epithelial Trx1 promotes BPD pathogenesis. Trx1 floxed mice (Trx1fl) were bred to mice expressing cre recombinase driven by the surfactant protein C promoter (sftpc-cre) to generate a mouse with Trx1 deficient lung epithelial cells. Although expected genotypic ratios were detected at birth, lethality was noted in Trx1fl/fl;sftpc-cre mice as early as 14 days of age. The LD50 for Trx1 deficient mice was 20 days old, while Trx1 heterozygote littermates appeared normal (p" @default.
- W2898771888 created "2018-11-09" @default.
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- W2898771888 date "2018-11-01" @default.
- W2898771888 modified "2023-09-27" @default.
- W2898771888 title "Impairment of thioredoxin 1 disrupts perinatal alveolar development" @default.
- W2898771888 doi "https://doi.org/10.1016/j.freeradbiomed.2018.10.280" @default.
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