McNamara, Coleen A.
Primary Appointment
Professor of Medicine/Cardiovascular Division, Beirne B. Carter Professor of Immunology and Director of the Beirne B. Carter Center for Immunology Research, Medicine: Cardiovascular Medicine
Education
- Fellowship, Cardiovascular Medicine, University of Virginia
- MD, , Medical College of Ohio
- Residency, Internal Medicine, University of Virginia
Contact Information
PO Box 801386
Telephone: 434-243-5854
Fax: 434-924-1221
Email: cam8c@virginia.edu
Website: https://www.immunology.virginia.edu/McNamara/
Research Disciplines
Biotechnology, Cardiovascular Biology, Immunology, Molecular Biology, Physiology, Translational Science
Research Interests
Immune System Regulation of Cardiometabolic Disease
Research Description
In recent years, obesity and diabetes have reached epidemic proportions. These diseases have many health consequences including stroke, heart attack and peripheral vascular disease. Common to all of these is atherosclerosis, which is the process by which lipids, cells and fibrous elements accumulate within the walls of arteries. Coordinated gene expression is essential to maintain normal vascular tissue structure and function and many transcription factors regulate these processes.
Our lab has recently identified the transcription factor Id3 as a major regulator of atherosclerosis and obesity. We have discovered that Id3 regulates the homing of B cells to the vasculature and that the loss of Id3 results in increased plaque formation. In ongoing research, we are utilizing different molecular imaging modalities to further explore and quantify the trafficking of B cells to the vessel wall and pursuing molecular strategies to further elucidate the mechanism by which Id3 affects the function of B cells in atherosclerosis.
In addition, studies from our lab have shown an important role for Id3 in the regulation of visceral adiposity. We have demonstrated the role of Id3 in the transcriptional regulation of adiponectin (an anti-inflammatory cytokine produced by adipocytes). Further studies are underway to investigate the mechanisms whereby Id3 deletion protects from high fat diet-induced obesity and glucose intolerance.