ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Thioredoxin-deficient mice, a novel phenotype sensitive to ambient air and hypersensitive to hyperoxia-induced lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Thioredoxin: an antioxidant, a therapeutic target and a possible biomarker.Pediatric research · 2024Article
- Insights into the Multifaceted Roles of Thioredoxin-1 System: Exploring Knockout Murine Models.Biology · 2024Review
- The Importance of Thioredoxin-1 in Health and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- S-Denitrosylation: A Crosstalk between Glutathione and Redoxin Systems.Antioxidants (Basel, Switzerland) · 2022Review
- Thioredoxin Prevents Loss of UCP2 in Hyperoxia via MKK4-p38 MAPK-PGC1α Signaling and Limits Oxygen Toxicity.American journal of respiratory cell and molecular biology · 2022Article
- Chaperone-Mediated Autophagy of eNOS in Myocardial Ischemia-Reperfusion Injury.Circulation research · 2021Article
- Thioredoxin deficiency exacerbates vascular dysfunction during diet-induced obesity in small mesenteric artery in mice.Microcirculation (New York, N.Y. : 1994) · 2021Article
- Hyperoxia and Lungs: What We Have Learned From Animal Models.Frontiers in medicine · 2021Review
- Molecular Basis for the Interactions of Human Thioredoxins with Their Respective Reductases.Oxidative medicine and cellular longevity · 2021Article
- Attenuation of Hyperoxic Lung Injury in Newborn Thioredoxin-1-Overexpressing Mice through the Suppression of Proinflammatory Cytokine mRNA Expression.Biomedicines · 2020Article
- Short-duration hyperoxia causes genotoxicity in mouse lungs: protection by volatile anesthetic isoflurane.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Role of Thioredoxin in Age-Related Hypertension.Current hypertension reports · 2018Review
- Intermittent Hypoxia Activates Duration-Dependent Protective and Injurious Mechanisms in Mouse Lung Endothelial Cells.Frontiers in physiology · 2018Article
- Thioredoxin reverses age-related hypertension by chronically improving vascular redox and restoring eNOS function.Science translational medicine · 2017Article
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- A novel mouse model for the identification of thioredoxin-1 protein interactions.Free radical biology & medicine · 2016Article
- Paradoxical Roles of Antioxidant Enzymes: Basic Mechanisms and Health Implications.Physiological reviews · 2016Review
- Thioredoxin Activates MKK4-NFκB Pathway in a Redox-dependent Manner to Control Manganese Superoxide Dismutase Gene Expression in Endothelial Cells.The Journal of biological chemistry · 2015Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Pulmonary oxygen toxicity is a major clinical problem for patients undergoing supplemental oxygen therapy. Thioredoxin (Trx) is an endogenous antioxidant protein that regenerates oxidatively inactivated proteins. We examined how Trx contributes to oxygen tolerance by creating transgenic mice with decreased levels of functional thioredoxin (dnTrx-Tg) using a dominant-negative approach. These mice showed decreased Trx activity in the lung although the expression of mutant protein is three times higher than the wild-type mice. Additionally, we found that these mice showed increased oxidation of endogenous Trx in room air. When exposed to hyperoxia (>90% O2) for 4 days, they failed to recover and showed significant mortality. Even in normal oxygen levels, these mice displayed a significant decrease in aconitase and NADH dehydrogenase activities, decreased mitochondrial energy metabolism, increased p53 and Gadd45α expression, and increased synthesis of proinflammatory cytokines. These effects were further increased by hyperoxia. We also generated mice overexpressing Trx (Trx-Tg) and found they maintained lung redox balance during exposure to high oxygen and thus were resistant to hyperoxia-induced lung injury. These mice had increased levels of reduced Trx in the lung in normoxia as well as hyperoxia. Furthermore, the levels of aconitase and NADH dehydrogenase activities were maintained in these mice concomitant with maintenance of mitochondrial energy metabolism. The genotoxic stress markers such as p53 or Gadd45α remained in significantly lower levels in hyperoxia compared with dnTrx-Tg or wild-type mice. These studies establish that mice deficient in functional Trx exhibit a phenotype of sensitivity to ambient air and hypersensitivity to hyperoxia.
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