Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 285, Issue 1, Pages L250-L257Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00387.2002
Keywords
hyperoxia; mitogen-activated protein kinase; oxidative stress; stress response; oxygen toxicity; apoptosis
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Funding
- NHLBI NIH HHS [HL-55330, HL-60234] Funding Source: Medline
- NIAID NIH HHS [AI-42365] Funding Source: Medline
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Hyperoxia generates an oxidative stress in the mouse lung, which activates the major stress-inducible kinase pathways, including c-Jun NH2-terminal kinase (JNK). We examined the effect of Jnk1 gene deletion on in vivo responses to hyperoxia in mice. The survival of Jnk1(-/-) mice was reduced relative to wild-type mice after exposure to continuous hyperoxia. Jnk1(-/-) mice displayed higher protein concentration in bronchoalveolar lavage (BAL) fluid and increased expression of heme oxygenase-1, a stress-inducible gene, after 65 h of hyperoxia. Contrary to other markers of injury, the leukocyte count in BAL fluid of Jnk1(-/-) mice was markedly diminished relative to that of wild-type mice. The decrease in BAL leukocyte count was not associated with any decrease in lung myeloperoxidase activity at baseline or after hyperoxia treatment. Pretreatment with inhaled lipopolysaccharide increased BAL neutrophil content and extended hyperoxia survival time to a similar extent in Jnk1(-/-) and wild-type mice. Associated with increased mortality, Jnk1(-/-) mice had increased pulmonary epithelial cell apoptosis after exposure to hyperoxia compared with wild-type mice. These results indicate that JNK pathways participate in adaptive responses to hyperoxia in mice.
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