Results of the study, which examined mice lacking Endothelial NO Synthase (eNOS), a gene important in blood vessel growth, show that offspring of these animals had major defects in their lung development which resulted in respiratory distress and death.
"We found that the lungs of eNOS deficient mice share the same features as newborns with a fatal condition known as Alevolar Capillary Dysplasia (ACD)," says Dr. Duncan Stewart, Chief of Cardiology, and Associate Director, Basic Science Research, St. Michael's Hospital and the Dexter Man Chair of Cardiology, University of Toronto. "This discovery opens up a door into the possible cause of ACD. Knowing that there is a defect in vessel formation in the lung, we can examine potential therapies for ACD, including using techniques previously used for heart disease such as stem cells and gene therapy to stimulate the growth of blood vessels in the lung."
Infants born with ACD, a rare disease with no known cause or cure, develop respiratory distress and quickly become critically ill. The condition is always fatal. The small blood vessels and capillaries in the lungs are not properly formed and the lungs typically show a misalignment of the pulmonary veins.
At St. Michael's Hospital, Dr. Stewart and Robin Han, Research Associate, studied genetically engineered mice lacking the eNOS gene to determine the cause of neonatal death in the mutant animals' offspring. They discovered that this deficiency caused major defects in the lung, resulting in respiratory distress and death. Tests showed that small blood vessels and capillaries were not formed properly and there was
Contact: Tracy MacIsaac
University of Toronto