Patched homolog 1 (PTCH1) variants have been identified in genome wide association studies for chronic obstructive pulmonary disease (COPD); however, its biological role was unclear.
Using lung tissues from healthy participants and COPD patients, Dr. Anthony Tam, a postdoc in Dr. Sin’s group and their team studied how the expression of PTCH1 as well as the morphology of airway epithelial cells differs between control and diseased tissues. PTCH1 was found to be upregulated in COPD airways and may upregulate mucous production, which is associated with COPD disease progression. In animal studies, knocking out PTCH1 resulted in attenuated wound closure and reduced mucous expression.
For COPD patients, excess mucous production and cough are important symptoms that are not currently targeted by available therapies. This study not only provides important insight into the underlying biological mechanism of COPD pathology, but also suggests that PTCH1 may be an important target to reduce symptoms for COPD patients.
Read the full study published in Scientific Reports.