Our labs study various aspects of thoracic and cardiovascular surgery with a focus on  post-transplant lung ischemia-reperfusion (IR) injury, immunology, and aneurysm formation.

Our primary projects include:

Lung IR Injury - Role of T cells and IL-17.  CD4+ T cells are key initiators of lung IR injury. This project tests the overall hypothesis that IR injury is initiated through iNKT cell activation via production of IL-17 and NADPH oxidase-dependent oxidative stress.

Lung IR Injury - Adenosine Receptor Activation.  One anti-inflammatory mechanism involves adenosine production which acts through four adenosine receptors: A1, A2A, A2B, and A3. This project tests the role of each adenosine receptor in lung IR injury using an in vivo muring model.

RAGE & IR Injury. The receptor for advanced glycation end products (RAGE) is a ubiquitous, multiligand receptor implicated in a variety of pathological conditions such as diabetes and its complications, cancer, cardiovascular disease and inflammation. We are studying the role of RAGE signaling via HMGB1 in lung IR injury.

Protection of Transplanted Lungs by Adenosine A2A Receptor Activation. This project, using a pig lung transplant model, tests the hypothesis that adenosine A2A receptor activation in the donor lung or in combination with other receptor agonists provides superior protection from IR injury.

Ex Vivo Lung Perfusion (EVLP). This project uses EVLP as a platform for pharmacologic delivery of A2AR agonist to test the overall hypothesis that EVLP with concomitant A2AR agonist treatment will prevent IR injury and rehabilitate non-heart beating donor (NHBD) lungs.

Aortic Aneurysm Formation.  We are investigating mechanisms of aneurysm formation including identification of smooth muscle cell (SMC) phenotype during aneurysm formation and the role of IL-1β signaling in SMC phenotypic switching.

Transplantation & Immunology. Our lab studies mechanisms of cardiothoracic transplant rejection with a current focus on adenosine signaling. We use various models including murine heterotopic and orthotopic tracheal transplant models of chronic rejection, an orthotopic heart transplant model, and the left lung hilar clamp model of lung IR injury.

Compensatory Lung Growth.  Pneumonectomy results in rapid compensatory growth of the remaining lung in experimental animals. We are studying mechanisms involved in this growth including the role of angiogenesis, angiogenic growth factors, and epithelial cell proliferation.

Lung Injury after Cardiopulmonary Bypass.  Cardiopulmonary bypass (CPB) is used to support the whole body while the heart is stopped, and it diverts blood away from the heart and lungs and subsequently oxygenates and re-circulates blood through the body. Lung injury after CPB is common, and we are studying mechanisms of this injury and ways to prevent such injury.