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Sunday, September 27, 2020  

A protein in the lungs may cause some smokers to develop lung damagePublished 5/25/2010

AURORA, Colo. (May 18, 2010) – A protein produced in lung cells may be the reason cigarette smoke injures the lungs. Cigarette smoking and exposure to second-hand smoke are responsible for many devastating lung diseases. The most common, chronic obstructive pulmonary disease (also known as COPD) and lung cancer, kill approximately 250,000 Americans every year. Unfortunately, there are no effective treatments for the main manifestations of COPD, emphysema (in which the lung is destroyed leaving large empty holes) and chronic bronchitis. For these reasons, patients with COPD are short of breath, frequently suffer infections (as with the flu), and are incapable of maintaining their physical strength during everyday activities, such as climbing a flight of stairs.

Rubin Tuder, MD, professor of Pulmonary Sciences and Critical Care Medicine and his colleagues in Israel, Baltimore, and Pittsburgh have discovered that a protein called Rtp801 that is produced in lung cells needs to be present for cigarette smoke to injure the lungs. When this protein is missing in mice, their lungs are remarkably protected against the damage caused by cigarette smoke. Tuder and colleagues found that the lungs of individuals who have smoked and those who have COPD show increased levels of this damaging protein. Their findings indicate that it is possible that an individual’s susceptibility to lung disease due to cigarette smoke may reside on the levels of Rtp801 induced by cigarette smoke.

Stresses such as cigarette smoke activate products of genes, such as Rtp801, that usually help cells compensate and survive if they are depleted of oxygen or nutrients. But with cigarette smoke, activation of Rtp801 is detrimental to the lung cells. Rtp801 also inhibits a key molecule called mTOR, which regulates cell growth when key nutrients are available. Low mTOR levels may decrease the lung’s ability to fend off the toxic effects of cigarette smoke.

"This study suggests that blocking Rtp801 could be a potential therapy for COPD. We also found how Rtp801 may be detrimental to the lung, paving the way for the chance of discovery of other important molecules which can be used to develop new treatments for this disease. Our findings may also be important to better treat other lung diseases in children, in which the lung fails to completely grow in premature babies who are put in incubators," said Tuder.

This paper will appear in the June issue of the medical journal Nature Medicine.

Faculty at the University of Colorado School of Medicine work to advance science and improve care. These faculty members include physicians, educators and scientists at University of Colorado Hospital, The Children’s Hospital, Denver Health, National Jewish Health, and the Denver Veterans Affairs Medical Center. Degrees offered by the UC School of Medicine include doctor of medicine, doctor of physical therapy, and masters of physician assistant studies. The School is located on the University of Colorado’s Anschutz Medical Campus, one of four campuses in the University of Colorado system. For additional news and information, please visit the UC Denver newsroom online.

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