Unique Gene Finding Related to COPD, Asthma, and Certain Cancers

Novel treatments for pulmonary conditions, such as asthma and chronic obstructive pulmonary disease (COPD), may be in the cards with new research findings.

Researchers from the Washington University School of Medicine in St. Louis (WUSTL) discussed their study highlighting a protein linked to mucus production in eLife.

Published on March 17, investigators documented calcium-activated chloride channel regulator 1 (CLCA1), a protein which came into interest two decades ago but until now was misclassified as a chloride channel.

“These results suggest cooperative roles for CLCA and TMEM16 proteins in influencing the physiology of multiple tissues, and the pathology of multiple diseases, including asthma, COPD, cystic fibrosis, and certain cancers,” the authors wrote.

The study also introduced a channel called TMEM16A, which was shown to increase in proportions similar to CLCA1 production. Previous studies determined large quantities of TMEM16A caused excess production of mucus.

“We don’t think that CLCA1 actually opens the channel. In fact, the channel can function without CLCA1,” Senior Author Thomas J. Brett, PhD, assistant professor of medicine at WUSTL said in a news release. “We think it simply keeps the channel on the surface of the cells for a longer period of time. The reason you get more current is you have more channels there. You’re just accumulating more holes for the ions to travel through. This is a unique finding. We don’t know of any other examples of this type of interaction between a protein and a channel.”

He also commented that the team is interested in further alleviating and investigating mucus production occurring in several conditions.

“On the flip side, these channel currents may be able to compensate for the genetic defect in cystic fibrosis, which causes mucus that is too thick and sticky,” Brett said. “In this case, we may be interested in activating them or dialing them up.”