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University of Cincinnati Academic Health Center
Publish Date: 11/13/01
Media Contact: AHC Public Relations, (513) 558-4553
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Findings Published on New Asthma Gene Identification

Cincinnati--A team of researchers led by Anil Menon, PhD, associate professor of molecular genetics, University of Cincinnati (UC) College of Medicine, has identified the gene for Aquaporin 5, a mercury sensitive water channel found in certain cells of the lung and elsewhere in the body, as a new candidate for susceptibility to asthma-related hypersensitivity of the airways. The team of researchers included efforts from Jeffrey Whitsett, MD, UC professor of pediatrics and director of the Pulmonary Biology/Neonatology at the Children's Hospital Medical Center (CHMC) in Cincinnati. Whitsett is well known for his research on surfactant, a detergent which helps premature babies breathe. The research team also included scientists that work with Stephen Liggett, MD, a professor and director of UC's Pulmonary Critical Care Division of Internal Medicine who is famous for asthma gene research. Other scientists that work under the direction of Richard Paul, PhD, a professor and expert in smooth muscle biology, contributed to these findings. Their data, reported in Proceedings of the National Academy of Sciences, (PNAS) article #2733, are the first to demonstrate a physiological role for Aquaporin 5 in controlling airway responsiveness and constriction of the bronchial tubes leading from the trachea to the lungs.

The authors report that genetically engineered mice who have the Aquaporin 5 gene "knocked-out" or lacking, respond to both inhaled and injected chemical stimulants with significantly more bronchial constriction than do mice with normal amounts of Aquaporin 5. They also show that normal mice have Aquaporin 5 in several different types of cells than previously thought, including a second type of lung cell and cells lining the trachea and bronchial tubes.

Previous genetic studies aimed at identifying the chromosomal location of potential genes for airway hypersensitivity associated with asthma have defined segments of human chromosome (#12q) that relate to mouse chromosome (#15), and found that both contain the gene for Aquaporin 5. Together, the physiological and genetic findings suggest that mutations in the gene for Aquaporin 5 may contribute to the development of some forms of asthma.

Menon said, "This is an example of a very successful collaboration that involved a team of outstanding trainees and senior investigators at UC and Children's Hospital." According to Menon, who is also a member of the UC Center for Environmental Genetics, this research team combined the efforts of the following Cincinnati researchers:

 

  • Carissa Krane, MD, PhD, UC molecular genetics, who played a key role in developing the aquaporin knock-out mouse;
  • Jennifer Towne, PhD, UC molecular genetics, who developed the antibodies for the aquaporin protein;
  • Dennis McGraw, MD, an associate professor, UC Internal Medicine-Pulmonary Critical Care;
  • Susan Wert, PhD, a research assistant professor in pediatrics-pulmonary biology at the UC College of Medicine and the Children's Hospital Medical Center in Cincinnati;
  • Christopher Fortner, PhD, a UC molecular and cellular physiology research assistant professor who worked in vascular biology.

 

"The local team of researchers listed above were also assisted by the efforts of John Lorenz, PhD, an expert physiologist and Arthur Hand, PhD, an expert electron microscopist, at the University of Connecticut," Menon said. This work was supported by the National Heart, Lung, and Blood Institute, the National Institute of Environmental Health Sciences, and the Cystic Fibrosis Foundation. To see the article published, log onto the National Academy of Sciences website at www.pnas.org.



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