RESEARCH INTERESTS
Research in the Tilley lab focuses on G protein-coupled receptor (GPCR)-mediated regulation of cardiac function, inflammation and remodeling during HF or following injury. The lab’s work has evolved from the initial elucidation of novel β-adrenergic receptor signaling mechanisms impacting heart function and remodeling to understanding their role in regulating cardio-immunological responses to acute and chronic stress. In addition, they are at the forefront of elucidating the roles of previously unrecognized cardiac-expressed adhesion GPCRs (aGPCRs) to uncover novel pharmacologic targets for HF and cardiomyopathies using complimentary molecular pharmacology and cardiac pathophysiology approaches. Dr. Tilley’s cardiac pharmacology achievements have been recognized through his receipt of the George B. Koelle Award from the Mid-Atlantic Pharmacology Society and being honored as a Fellow of the American Heart Association. His leadership experience spans internal activities, including as a former Medical Faculty Senate President and currently as Associate Dean, Faculty Affairs, as well as external activities, including as past-President of the Mid-Atlantic Pharmacology Society (MAPS) chapter of the American Society for Pharmacology and Experimental Therapeutics (ASPET) and currently as Chair of the Cardiovascular Pharmacology division of ASPET.
Current Projects
Structural determinants of EGFR effects on cardiac function and remodeling
The epidermal growth factor receptor (EGFR) has long been implicated as a pro-hypertrophic signaling node downstream of neurohormone GPCRs, however we recently discovered that it also acts to maintain cardiac contractile homeostasis. Understanding the specific molecular requirements controlling these processes could provide novel insight into how to dissociate EGFR-dependent hypertrophy from contractile homeostasis as a novel therapeutic strategy for chronic HF.
βAR-dependent regulation of leukocytes in acute cardiac injury
The goal of this project is to define how β2-adrenergic receptor (β2AR) regulates leukocyte function and survival, not only to attain a fundamental understanding of the mechanisms and influence of β2AR signaling on the early immune response to cardiac injury, but also to determine whether β2AR-selective therapeutics would offer fine-tuned strategies to regulate ischemic injury-induced remodeling and survival outcomes.
Leukocyte-dependent regulation of cardiorenal syndrome
Renal dysfunction is a strong independent predictor for poor prognosis in HF patients, which manifests as cardiorenal syndrome (CRS), therefore understanding how renal fibrosis and dysfunction are mediated during the development and progression of CRS is essential to designing therapeutic strategies to ameliorate this condition. The goals of this project are to define the role of leukocytes in mediating CRS development and progression, characterize the molecular pathways by which they do so and test how their modulation impacts the development of renal fibrosis and dysfunction.
EDUCATION, TRAINING & CREDENTIALS
- Postdoctoral Fellowship, Duke University Medical Center, Division of Cardiology, Durham, NC, 2008
- PhD, Queen's University at Kingston, Ontario, Canada, 2005
- BScH, Life Sciences SSP, Queen's University at Kingston, Ontario, Canada, 1999
MEMBERSHIPS
- American Society for Pharmacology and Experimental Therapeutics
- American Heart Association
- International Society for Heart Research, American Section
PUBLICATIONS