Stat-3 is required for pulmonary homeostasis during hyperoxia

Acute lung injury syndromes remain common causes of morbidity and mortality in adults and children. Cellular and physiologic mechanisms maintaining pulmonary homeostasis during lung injury remain poorly understood. In the present study, the Stat-3 gene was selectively deleted in respiratory epitheli...

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Veröffentlicht in:	The Journal of clinical investigation 2004-01, Vol.113 (1), p.28-37
Hauptverfasser:	Hokuto, Isamu, Ikegami, Machiko, Yoshida, Mitsuhiro, Takeda, Kiyoshi, Akira, Shizuo, Perl, Anne-Karina T, Hull, William M, Wert, Susan E, Whitsett, Jeffrey A
Format:	Artikel
Sprache:	eng
Schlagworte:	Adult Animals Apoptosis Base Sequence Biomedical research Child Cytokines DNA Primers DNA-Binding Proteins - deficiency DNA-Binding Proteins - genetics DNA-Binding Proteins - physiology Growth factors Histology Homeostasis Humans Hyperoxia Hypoxia - physiopathology Immunohistochemistry Kinases Laboratories Lung - pathology Lung - physiology Lung - physiopathology Lung Diseases - genetics Lung Diseases - pathology Lung Diseases - physiopathology Mice Mice, Knockout Mice, Transgenic Morphogenesis Phosphorylation Polymerase Chain Reaction Proteins Pulmonary Surfactant-Associated Protein B - physiology Respiratory distress syndrome Respiratory Mucosa - physiology RNA, Messenger - genetics Severe acute respiratory syndrome STAT3 Transcription Factor Surfactants Trans-Activators - deficiency Trans-Activators - genetics Trans-Activators - physiology Transcription, Genetic
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