Genetically knocking the protein out of a specialized strain of mouse that models chronic lung disease resulted in higher levels of inflammation, mucus, and tissue damage in the lungs as well as early death in the mice lacking the protein, researchers found.
A separate commentary by University of North Carolina researchers in the same issue of the journal calls the finding "surprising and important" in light of the fact that suppressing the protein is being investigated as a potential treatment for asthma.
"Some believe this receptor protein plays a detrimental role and if you block it, you could improve asthma. This study shows that if you remove this protein from a diseased lung, you'll make lung inflammation and damage worse," said senior author Michael R. Blackburn, Ph.D., associate professor of biochemistry and molecular biology at the UT Medical School at Houston. By completely removing the protein, known as the A1 adenosine receptor, from a diseased line of mice, "we can be sure that what we are dealing with are A1 receptor responses," Blackburn said. "In our model of adenosine dependent lung disease, it appears that the A1 receptor plays an important role turning on anti-inflammatory and tissue protective pathways."
The A1 receptor also has been associated with bronchoconstriction in asthmatic airways by other researchers.
The receptor, A1AR for short, is one of four proteins found on cell surfaces that connect with the signaling molecule adenosine. Adenosine, a byproduct of stress and tis
Contact: Scott Merville
University of Texas Health Science Center at Houston