University researchers have generated new mice that could lead to better, safer aspirin and other nonsteroidal anti-inflammatory drugs.
Scientists from the School of Medicine and the National Institute of Environmental Health Sciences, who teamed to develop the mice, expect drug companies to be very interested in the animals.
The researchers have designed and bred two strains of mice lacking one or the other of two key enzymes--COX-1 and COX-2--on which aspirin, ibuprofen and other nonsteroidal anti-inflammatories work. The rodents will enable scientists to learn more about how genes control pain and inflammation.
Using a gene-targeting technique pioneered by Oliver Smithies, Excellence professor of pathology, researchers inserted the defective genetic material into mouse cells. Those cells were then incorporated into otherwise normal mice, and the teams bred successive generations of the rodents in which either the COX-1 or COX-2 gene was eliminated.
Mice lacking COX-2 were born normal, but as they grew, they developed severe kidney problems, Morham said. They had no decrease in inflammatory response, however, which led the scientists to conclude that COX-2 is not as necessary for inflammation as previously thought.
On the other hand, scientists found the animals lacking COX-1 to be surprisingly healthy.
The scientific journal Cell included two reports on the research efforts. Authors include Robert Langenbach, senior scientist at NIEHS, and Carolina team members Smithies; Scott G. Morham, an American Cancer Society postdoctoral fellow in pathology; and J. Charles Jenrette, professor of pathology .
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