Gene Tied to Infants' Lung Maturation
Deleting it in mice caused fatal respiratory distress, study says
THURSDAY, Dec. 4, 2008 (HealthDay News) -- A gene vital to lung development in newborn mice might be key to finding ways to handle respiratory problems in human infants, a new report says.
Researchers at Cincinnati Children's Hospital Medical Center found that if they deleted the Foxm1 gene from embryonic mice, lungs developed but did not mature fully or produce two critical proteins that line lung tissues and prevent them from collapsing. As a result, the mice died shortly after birth from respiratory distress.
"Our findings demonstrate the Foxm1 gene's central importance to lung maturation and surfactant production in mice," study senior investigator Dr. Vladimir Kalinichenko, a physician in the division of pulmonary biology at Cincinnati Children's, said in a news release issued by the hospital. "Ultimately, this information is important to newborn survival, as infants must breathe on their own at birth instead of getting oxygen from the mother's umbilical cord blood."
The findings were published online in the Proceedings of the National Academy of Sciences.
In the study, Kalinichenko and his colleagues wrote that "identifying critical regulators of lung maturation, such as Foxm1, may provide novel strategies for diagnosis, prevention and treatment of respiratory distress syndrome (RDS) in preterm infants."
The researchers are now looking for drugs that can activate Foxm1 in hopes of developing drugs that treat diseases involving Foxm1 deficiency, Kalinichenko said. Such a find could help treat premature babies with respiratory distress syndrome by inducing lung maturation and surfactant production.
The U.S. National Library of Medicine has more about respiratory distress syndrome.