In a development that could lead to a novel approach to the treatment of a devastating lung disease, biochemists at The University of Texas Health Science Center at Houston report they are the first to link the osteopontin (OPN) protein to chronic obstructive pulmonary disease (COPD). Findings appear online and will be in the January 2010 print issue of The FASEB Journal, the journal of The Federation of American Societies for Experimental Biology.
More than 12 million Americans are currently diagnosed with this incurable illness, which is the fourth leading cause of death, the National Heart Lung and Blood Institute reports. In the United States, the term COPD includes two main conditions - emphysema and chronic obstructive bronchitis.
The researchers were able to prevent COPD features in a mouse model by genetically removing osteopontin. To gauge the applicability of their findings to humans, the investigators analyzed the airways of people with COPD and found elevated levels of the protein.
"This is an important crossover study," said Michael Blackburn, Ph.D., the study's senior author and professor in the Department of Biochemistry and Molecular Biology at The University of Texas Medical School at Houston. "Because we can show osteopontin is elevated in people with COPD, this suggests that osteopontin could serve as both an indicator of disease progression and a therapeutic target."
In the study, researchers induced COPD features in mice and then compared symptoms experienced by mice with osteopontin and those without. The mice without the protein had less inflammation and lung disease. "The lack of osteopontin in the mice prevented the COPD features," said Daniel Schneider, the study's lead author and an M.D./Ph.D. candidate at the UT Health Science Center at Houston.
"This paper reveals exciting new information on the pathogenetic mechanisms involved in the development of chronic obstructive pulmonary
|Contact: Robert Cahill|
University of Texas Health Science Center at Houston