Alpha-1 Foundation Awards Two Research Grants with Support from Talecris Biotherapeutics, Inc.
MIAMI, Jan. 5, 2011 /PRNewswire/ -- The Alpha-1 Foundation announced today that it has awarded two research grants to investigators whose research will contribute to our understanding of the causes and mechanisms that give rise to lung disease. The first grant will investigate how cigarette smoke promotes the onset of emphysema through the destruction of elastic fibers in the lung, and how the alpha(1)-proteinase inhibitor (A1PI) protein protects the elastic fibers from degradation. The second grant will evaluate how the alpha(1)-proteinase inhibitor (A1PI) interacts with lung cells and plasma membranes. A1PI plays an essential role in the lung, limiting the activity of destructive enzymes released by inflammatory cells. In addition, environmental and genetic factors can reduce levels of A1PI, which can then lead to emphysema.
The annual research grants are part of the Alpha-1 Foundation's ongoing commitment to increase the understanding of alpha-1 antitrypsin deficiency, a genetic disorder in which low levels of the A1PI protein can result in liver damage and emphysema. The 2010 research grants were awarded to Kamal Akhtar, PhD, of the Washington University School of Medicine, St. Louis, MO and Irina Petrache, MD, of Indiana University, Indianapolis, IN.
Akhtar's team will study how the destructive oxidants in cigarette smoke cause two-fold damage in the lungs by degrading elastic fibers that allow the lungs to stretch and recoil and by damaging A1PI so it does not function correctly. A1PI normally acts in the lungs by inhibiting and neutralizing inflammatory enzymes that can break down elastic fibers.
Petrache's team will study how A1PI interacts with lung cells, and how defects in the structure of A1PI can affect these functions. Specifically, Petrache will study variations to the alpha-1 protein made by removing its sugar molecules to determine how this change affects the ability of A1PI to enter the cells and interact with their membran