ArticleMolecular and cellular biochemistry2015
Autophagy regulates hyperoxia-induced intracellular accumulation of surfactant protein C in alveolar type II cells.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Epidermal growth factor receptor regulates Beclin-1 in hyperoxic acute lung injury.BMJ open respiratory research · 2026Article
- The dual role of mTOR signaling in lung development and adult lung diseases.Cell & bioscience · 2025Review
- The Role of Cuproptosis in Hyperoxia-Induced Lung Injury and Its Potential for Treatment.Journal of inflammation research · 2025Article
- Hyperoxia reduces STX17 expression and inhibits the autophagic flux in alveolar type II epithelial cells in newborn rats.International journal of molecular medicine · 2020Article
- Review
- The Impact of Moderate Chronic Hypoxia and Hyperoxia on the Level of Apoptotic and Autophagic Proteins in Myocardial Tissue.Oxidative medicine and cellular longevity · 2018Article
- Early injury of the neonatal lung contributes to premature lung aging: a hypothesis.Molecular and cellular pediatrics · 2016Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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Abstract
Surfactant protein C (SP-C) deficiency is a risk factor for hyperoxia-induced bronchopulmonary dysplasia in newborn infants. However, the role of SP-C deficiency in the process is unclear. Here, using neonatal rat BPD model and MLE-12, mouse alveolar epithelial type II cell, we examined the changes of SP-C levels during hyperoxia. Immunohistochemistry, immunofluorescence, and ELISA analysis showed SP-C accumulation in alveolar epithelial type II cells. Electron microscopy further demonstrated the accumulation of lamellar bodies and the co-localization of lamellar bodies with autophagosomes in the cytoplasm of alveolar epithelial type II cells. The inhibition of autophagy with 3-Methyladenine and knockdown of Atg7 abolished hyperoxia-induced SP-C accumulation in the cytoplasm. Furthermore, inhibition of JNK signaling with SP600125 suppressed hyperoxia-induced Atg7 expression and SP-C accumulation. These findings suggest that hyperoxia triggers autophagy via JNK signaling-mediated Atg7 expression, which promotes the accumulation of SP-C within alveolar epithelial type II cells. Our data provide a potential approach for hyperoxic lung injury therapy by targeted pharmacological inhibition of autophagic pathway.
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