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Pressure Controlled Ventilation to Induce Acute Lung Injury in Mice
Published on: May 5, 2011
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Adenosine promotes vascular barrier function in hyperoxic lung injury.
Jonathan Davies1, Harry Karmouty-Quintana2, Thuy T Le2
1Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.
Physiological Reports
|September 30, 2014
Summary
Elevated adenosine levels protect against hyperoxic lung injury by maintaining vascular barrier function. This protective effect is mediated by CD73 and ADORA2B signaling, preventing pulmonary edema.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Immunology
Background:
- Hyperoxic lung injury involves inflammation and edema due to high oxygen concentrations.
- Adenosine, generated by CD73, plays a protective role in acute injury via ADORA2B signaling.
- The role of adenosine in hyperoxic lung injury remains largely unexplored.
Purpose of the Study:
- To investigate the role of CD73-mediated adenosine signaling in hyperoxic lung injury.
- To determine if extracellular adenosine protects against hyperoxia-induced lung damage via ADORA2B.
Main Methods:
- Exposure of C57BL6, CD73(-/-), and Adora2B(-/-) mice to 95% oxygen.
- Assessment of pulmonary inflammation, edema, and lung histology.
- Measurement of lung adenosine levels and occludin expression.
Main Results:
- Hyperoxia induced lung injury with increased adenosine levels.
- Loss of CD73 or ADORA2B exacerbated pulmonary edema but not inflammation.
- Impaired vascular barrier function, indicated by decreased occludin, was observed in CD73(-/-) and Adora2B(-/-) mice.
Conclusions:
- Hyperoxic lung injury increases adenosine concentration.
- Adenosine protects vascular barrier integrity in hyperoxic lung injury through ADORA2B-dependent occludin regulation.
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