PITTSBURGH, March 26 Mutations in a gene may cause poor lung development in children, making them more vulnerable to diseases such as chronic obstructive pulmonary disease (COPD) later in life, say researchers at the University of Pittsburgh Graduate School of Public Health and the German Research Center for Environmental Health. Their study, published online in Physiological Genomics, measured expression levels of the gene and its variants in both mouse lungs and children ages 9 to 11.
Study authors, led by George Leikauf, Ph.D., professor of occupational and environmental health at the University of Pittsburgh Graduate School of Public Health, and Holger Schulz, M.D., professor of medicine at the Institute of Lung Biology and Disease, German Research Center for Environmental Health, Munich, focused on a gene called superoxide dismutase 3 (SOD3), previously shown to protect the lungs from the effects of asbestos and oxidative stress.
"People lose lung function as they age, so it's important to identify possible genetic targets that control healthy development of the lungs during childhood," said Dr. Leikauf.
Drs. Leikauf, Schulz and colleagues compared SOD3 expression levels in strains of mice with poor lung function to one with more efficient airways and lungs two times the size. As with people, the lungs of mice fully form as they mature to adulthood. The better-functioning strain maintained higher levels of SOD3 levels in these mice were four times higher at the final stage of lung development. They also found the presence of single nucleotide polymorphisms, or SNPs, variations in DNA sequences, in SOD3 that were linked to lung function in mice.
The researchers went on to assess SOD3 mutations in children ages 9 to 11 by testing for SNPs linked to lung function. After analyzing DNA from 1,555 children in Munich and Dresden who were part of the International Study of Asthma and Allergy in Children, they d
|Contact: Clare Collins|
University of Pittsburgh Schools of the Health Sciences