ArticleFree radical biology & medicine2011
Reactive oxygen species-dependent RhoA activation mediates collagen synthesis in hyperoxic lung fibrosis.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Epidermal growth factor receptor regulates Beclin-1 in hyperoxic acute lung injury.BMJ open respiratory research · 2026Article
- Caffeine Protects Against Hyperoxia-Induced Structural Lung Injury and Restores Alveolar Development in Neonatal Rats.Antioxidants (Basel, Switzerland) · 2025Article
- Impact of vitamin D on hyperoxic acute lung injury in neonatal mice.BMC pulmonary medicine · 2024Article
- Protective Effects of Resveratrol Against Airway Hyperreactivity, Oxidative Stress, and Lung Inflammation in a Rat Pup Model of Bronchopulmonary Dysplasia.Physiological research · 2024Article
- The RAAS Goodfellas in Cardiovascular System.Journal of clinical medicine · 2023Review
- Glutamine inhibits inflammation, oxidative stress, and apoptosis and ameliorates hyperoxic lung injury.Journal of physiology and biochemistry · 2023Article
- Endothelial to mesenchymal transition in neonatal hyperoxic lung injury: role of sex as a biological variable.Physiological genomics · 2023Article
- Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries.Antioxidants (Basel, Switzerland) · 2023Review
- Potential effect of amniotic fluid-derived stem cells on hyperoxia-induced pulmonary alveolar injury.Stem cell research & therapy · 2022Article
- Hyperoxia and modulation of pulmonary vascular and immune responses in COVID-19.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Application Prospects of Mesenchymal Stem Cell Therapy for Bronchopulmonary Dysplasia and the Challenges Encountered.BioMed research international · 2021Review
- Fucoidan attenuates hyperoxia-induced lung injury in newborn rats by mediating lung fibroblasts differentiate into myofibroblasts.Annals of translational medicine · 2020Article
- Epigenetic response to hyperoxia in the neonatal lung is sexually dimorphic.Redox biology · 2020Article
- Article
- Clinical importance ofJournal of thoracic disease · 2019Article
- Role ofOxidative medicine and cellular longevity · 2019Article
- Sex-specific differences in primary neonatal murine lung fibroblasts exposed to hyperoxia in vitro: implications for bronchopulmonary dysplasia.Physiological genomics · 2018Article
- TRPA1 channels: expression in non-neuronal murine lung tissues and dispensability for hyperoxia-induced alveolar epithelial hyperplasia.Pflugers Archiv : European journal of physiology · 2018Article
- [Preventive effect of caffeine on bronchopulmonary dysplasia in preterm infants].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018Review
- Primary culture of lung fibroblasts from hyperoxia-exposed rats and a proliferative characteristics study.Cytotechnology · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Lung fibrosis is an ultimate consequence of pulmonary oxygen toxicity in human and animal models. Excessive production and deposition of extracellular matrix proteins, e.g., collagen-I, is the most important feature of pulmonary fibrosis in hyperoxia-induced lung injury. In this study, we investigated the roles of RhoA and reactive oxygen species (ROS) in collagen-I synthesis in hyperoxic lung fibroblasts and in a mouse model of oxygen toxicity. Exposure of human lung fibroblasts to hyperoxia resulted in RhoA activation and an increase in collagen-I synthesis and cell proliferation. Inhibition of RhoA by C3 transferase CT-04, dominant-negative RhoA mutant T19N, or RhoA siRNA prevented hyperoxia-induced collagen-I synthesis. The constitutively active RhoA mutant Q63L mimicked the effect of hyperoxia on collagen-I expression. Moreover, the Rho kinase inhibitor Y27632 inhibited collagen-I synthesis in hyperoxic lung fibroblasts and fibrosis in mouse lungs after oxygen toxicity. Furthermore, the ROS scavenger tiron attenuated hyperoxia-induced increases in RhoA activation and collagen-I synthesis in lung fibroblasts and mouse lungs after oxygen toxicity. More importantly, we found that hyperoxia induced separation of guanine nucleotide dissociation inhibitor (GDI) from RhoA in lung fibroblasts and mouse lungs. Further, tiron prevented the separation of GDI from RhoA in hyperoxic lung fibroblasts and mouse lungs with oxygen toxicity. Together, these results indicate that ROS-induced separation of GDI from RhoA leads to RhoA activation with oxygen toxicity. ROS-dependent RhoA activation is responsible for the increase in collagen-I synthesis in hyperoxic lung fibroblasts and mouse lungs.
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