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Published on: October 19, 2013
Stat-3 is required for pulmonary homeostasis during hyperoxia
Isamu Hokuto1, Machiko Ikegami, Mitsuhiro Yoshida
1Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039, USA.
The Journal of Clinical Investigation
|January 1, 2004
Summary
Signal transducer and activator of transcription 3 (Stat-3) in lung epithelial cells is crucial for maintaining lung function during oxygen-induced lung injury. Deleting Stat-3 worsens acute lung injury and impairs surfactant production.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Cell Biology
Background:
- Acute lung injury (ALI) syndromes are significant causes of mortality.
- Mechanisms preserving lung homeostasis during ALI are not fully understood.
- The role of Signal transducer and activator of transcription 3 (Stat-3) in respiratory epithelial cells during lung injury requires elucidation.
Purpose of the Study:
- To investigate the role of Stat-3 in respiratory epithelial cells in maintaining lung homeostasis.
- To determine the impact of Stat-3 deletion on lung development and function.
- To assess the effect of Stat-3 deletion on lung injury response to hyperoxia.
Main Methods:
- Conditional deletion of the Stat-3 gene in respiratory epithelial cells using Cre-recombinase under the surfactant protein C promoter in mice.
- Assessment of lung morphogenesis and function.
- Exposure of mice to 95% oxygen to induce lung injury.
- Analysis of alveolar capillary leak, epithelial cell injury, inflammatory responses, and surfactant levels.
- Evaluation of survival and lung histology after treatment with exogenous surfactant protein B.
Main Results:
- Stat-3 deletion in respiratory epithelial cells did not affect prenatal lung development or postnatal lung function.
- Stat-3-deleted mice exhibited accelerated and severe lung injury, increased alveolar capillary leak, and acute respiratory distress upon hyperoxia exposure.
- Epithelial cell injury, inflammation, and surfactant protein/lipid deficiency were exacerbated in Stat-3-deleted mice.
- Surfactant protein B administration improved survival and lung histology in Stat-3-deleted mice during hyperoxia.
Conclusions:
- Stat-3 expression in respiratory epithelial cells is dispensable for lung formation.
- Stat-3 plays a critical role in maintaining pulmonary surfactant homeostasis.
- Stat-3 is essential for lung function and protection against oxygen-induced lung injury.
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