Alexandra C. Racanelli, MD, PhD

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide. Current therapy only treats symptoms but cannot stop progression of this debilitating disease. COPD is most associated with cigarette smoke and affects over 250 million people worldwide and the number of cases continue to rise. We have found evidence that dysfunction of blood vessels in the lung leads to the development of the type of lung destruction found in COPD. But little is known of how blood vessel damage leads to progressive lung destruction.We will use a mouse model of COPD and human lung cells to better understand how this dysfunction develops. We will focus on a protein called LRG1, to see if excessive levels cause blood vessel abnormalities that lead to development of COPD. These findings will lead to new therapies targeting blood vessel impairments causing COPD in the hopes of improving the lives of millions of patients.

Update:
Our studies this year focused on understanding the role of endothelial derived leucine-rich-2-alpha glycoprotein-1 (LRG1) in the development of COPD. We are using both animal and human studies for this purpose. We have established the genetically modified mouse lines and the emphysema models required for our studies. We have also learned new strategies to developed human lung alveolar organoids (three-dimensional tissue cultures that are derived from stem cells). Finally, we have measured LRG1 in plasma and urine obtained from non-smoker, smoker, mild/moderate COPD and severe COPD enrolled in the Subpopulations and Intermediate Outcome Measurements in COPD study (SPIROMICS).