| http://purl.uniprot.org/citations/27089175 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27089175 | http://www.w3.org/2000/01/rdf-schema#comment | "Oxygen toxicity and antioxidant deficiencies contribute to the development of bronchopulmonary dysplasia. Aurothioglucose (ATG) and auranofin potently inhibit thioredoxin reductase-1 (TrxR1), and TrxR1 disruption activates nuclear factor E2-related factor 2 (Nrf2), a regulator of endogenous antioxidant responses. We have shown previously that ATG safely and effectively prevents lung injury in adult murine models, likely via Nrf2-dependent mechanisms. The current studies tested the hypothesis that ATG would attenuate hyperoxia-induced lung developmental deficits in newborn mice. Newborn C3H/HeN mice were treated with a single dose of ATG or saline within 12 hours of birth and were exposed to either room air or hyperoxia (85% O2). In hyperoxia, ATG potently inhibited TrxR1 activity in newborn murine lungs, attenuated decreases in body weight, increased the transcription of Nrf2-regulated genes nicotinamide adenine dinucleotide phosphate reduced quinone oxidoreductase-1 (NQO1) and heme oxygenase 1, and attenuated alterations in alveolar development. To determine the impact of TrxR1 inhibition on Nrf2 activation in vitro, murine alveolar epithelial-12 cells were treated with auranofin, which inhibited TrxR1 activity, enhanced Nrf2 nuclear levels, and increased NQO1 and heme oxygenase 1 transcription. Our novel data indicate that a single injection of the TrxR1 inhibitor ATG attenuates hyperoxia-induced alterations in alveolar development in newborn mice. Furthermore, our data support a model in which the effects of ATG treatment likely involve Nrf2 activation, which is consistent with our findings in other lung injury models. We conclude that TrxR1 represents a novel therapeutic target to prevent oxygen-mediated neonatal lung injury."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.org/dc/terms/identifier | "doi:10.1165/rcmb.2015-0228oc"xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/author | "Li Q."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/author | "Ren C."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/author | "Velten M."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/author | "Wall S.B."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/author | "Rogers L.K."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/author | "Tipple T.E."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/author | "Hill C.L."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/author | "Locy M.L."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/name | "Am J Respir Cell Mol Biol"xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/pages | "419-428"xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/title | "Thioredoxin Reductase Inhibition Attenuates Neonatal Hyperoxic Lung Injury and Enhances Nuclear Factor E2-Related Factor 2 Activation."xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://purl.uniprot.org/core/volume | "55"xsd:string |
| http://purl.uniprot.org/citations/27089175 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/27089175 |
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| http://purl.uniprot.org/uniprot/Q91Y98 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/27089175 |