ArticleAmerican journal of physiology. Cell physiology2014
Dysregulation of CLOCK gene expression in hyperoxia-induced lung injury.
Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Traumatic brain injury-induced disruption of the circadian clock.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Effect of low-to-moderate hyperoxia on lung injury in preclinical animal models: a systematic review and meta-analysis.Intensive care medicine experimental · 2023Review
- Circadian clock molecule REV-ERBα regulates lung fibrotic progression through collagen stabilization.Nature communications · 2023Article
- Tight Junctions, the Epithelial Barrier, and Toll-like Receptor-4 During Lung Injury.Inflammation · 2022Review
- Lung fibrosis is induced in ADAR2 overexpressing mice via HuR-induced CTGF signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Expression Patterns of Clock Gene mRNAs and Clock Proteins in Human Psoriatic Skin Samples.International journal of molecular sciences · 2021Article
- Loss of circadian protection against influenza infection in adult mice exposed to hyperoxia as neonates.eLife · 2021Article
- It's about time: clocks in the developing lung.The Journal of clinical investigation · 2020Review
- Alda-1 Attenuates Hyperoxia-Induced Acute Lung Injury in Mice.Frontiers in pharmacology · 2020Article
- Fatigue, Sleep, and Autoimmune and Related Disorders.Frontiers in immunology · 2019Review
- Caffeine ameliorates hyperoxia-induced lung injury by protecting GCH1 function in neonatal rat pups.Pediatric research · 2017Article
- Deletion of P2X7 attenuates hyperoxia-induced acute lung injury via inflammasome suppression.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Article
- Circadian molecular clock in lung pathophysiology.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Enhanced Resolution of Hyperoxic Acute Lung Injury as a result of Aspirin Triggered Resolvin D1 Treatment.American journal of respiratory cell and molecular biology · 2015Article
- Adenovirus-mediated transfer of the SOCS-1 gene to mouse lung confers protection against hyperoxic acute lung injury.Free radical biology & medicine · 2015Article
- High level of oxygen treatment causes cardiotoxicity with arrhythmias and redox modulation.Toxicology and applied pharmacology · 2015Article
- Resolvins Decrease Oxidative Stress Mediated Macrophage and Epithelial Cell Interaction through Decreased Cytokine Secretion.PloS one · 2015Article
- Reactive oxygen species at the crossroads of inflammasome and inflammation.Frontiers in physiology · 2014Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Hyperoxic acute lung injury (HALI) is characterized by inflammation and epithelial cell death. CLOCK genes are master regulators of circadian rhythm also implicated in inflammation and lung diseases. However, the relationship of CLOCK genes in hyperoxia-induced lung injury has not been studied. This study will determine if HALI alters CLOCK gene expression. To test this, wild-type and NALP3(-/-) mice were exposed to room air or hyperoxia for 24, 48, or 72 h. In addition, mice were exposed to different concentrations of hyperoxia (50, 75, or 100% O2) or room air for 72 h. The mRNA and protein levels of lung CLOCK genes, based on quantitative PCR and Western blot analysis, respectively, and their target genes are significantly elevated in mice exposed to hyperoxia compared with controls. Alterations in CLOCK genes are associated with increased inflammatory markers in bronchoalveolar lavage fluid of hyperoxic mice compared with controls. Histological examination of mice lungs exposed to hyperoxia show increased inflammation and alveolar congestion compared with controls. Our results indicate sequential increase in CLOCK gene expression in lungs of mice exposed to hyperoxia compared with controls. Additionally, data suggest a dose-dependent increase in CLOCK gene expression with increased oxygen concentrations. To validate if the expression changes related to CLOCK genes are indeed associated with inflammation, NALP3(-/-) was introduced to analyze loss of function in inflammation. Western blot analysis showed significant CLOCK gene downregulation in NALP3(-/-) mice compared with wild-type controls. Together, our results demonstrate that hyperoxia-mediated lung inflammation is associated with alterations in CLOCK gene expression.
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Registered trials
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