Susan M. Lessner, Ph.D.
Research Assistant Professor
Phone: (803) 733-3233
Fax: (803) 733-1533
Lessner@gw.med.sc.edu
Lab Page under construction

Professional Experience

Research Interests

Dr. Lessner’s research interests center on vascular remodeling and angiogenesis (new blood vessel growth) in the contexts of atherosclerosis and tissue engineering. Vascular remodeling can be defined as any lasting change in the diameter, thickness, or structure of a mature blood vessel. In atherosclerosis, vascular remodeling acts as a compensatory mechanism to preserve blood flow in the face of plaque growth, which tends to cause stenosis or narrowing of the artery. However, vascular remodeling in atherosclerotic arteries has been correlated pathologically with plaque rupture, which leads to adverse clinical events such as heart attack and stroke. I am particularly interested in the role of matrix metalloproteinases (MMPs) in vascular remodeling and plaque vulnerability. MMPs are a class of enzymes which can degrade the extracellular matrix. We have shown in a mouse model of atherosclerosis that one of these enzymes, MMP-9, is required for vascular remodeling. Control of vascular remodeling is also important to the field of cardiovascular tissue engineering, since, once implanted in the body, engineered constructs are subject to the same types of cellular interactions as native tissues.

Another phenomenon which contributes to destabilization and rupture of atherosclerotic lesions is plaque angiogenesis. Like tumors, atherosclerotic plaques become hypoxic as they increase in thickness, due to oxygen transport limitations to the central core of the lesion. Tissue hypoxia promotes angiogenesis, or growth of new capillaries into the oxygen-starved region. I am interested in understanding both the fundamental biology of angiogenesis within atherosclerotic lesions as well as how angiogenesis contributes to plaque instability, using both in vitro and in vivo approaches.

While angiogenesis within atherosclerotic lesions may be harmful, there are other situations in which increasing angiogenesis would be beneficial. For example, promoting blood vessel growth into scaffolds used in tissue engineering is an essential strategy to ensure long-term integration and functioning of engineered tissues. Another current area of research in my lab involves delivery of angiogenic factors from tissue-engineered scaffolds. Confocal microscopy and other imaging modalities available through the Instrumentation Resource Facility are used to assess vascularization of implanted scaffolds in mouse models.

Professional Memberships

American Heart Association
American Chemical Society
Sigma Xi

Honors

Recent Publications

H.-J. Sung, C. E. Johnson, S. M. Lessner, R. Magid, D. N. Drury, and Z. S. Galis, “Matrix Metalloproteinase (MMP)-9 Facilitates Collagen Remodeling and Angiogenesis for Vascular Constructs,” Tissue Eng. (in press).

S. M. Lessner, D. E. Martinson, and Z. S. Galis, “Compensatory Vascular Remodeling during Atherosclerotic Lesion Growth Depends on Matrix Metalloproteinase-9 Activity,” Arterioscl. Thromb. Vasc. Biol., 24, 2123-2129 (2004).

S. M. Lessner and Z. S. Galis, “Matrix Metalloproteinases and Vascular Endothelium-Mononuclear Cell Close Encounters,” Trends Cardiovasc. Med., 14, 105-111 (2004).

S.-H. Kim, S. M. Lessner, Y. Sakurai, and Z. S. Galis, “Cyclophilin A as a Novel Biphasic Mediator of Endothelial Activation and Dysfunction,” Am. J. Pathol., 164, 1567-1574 (2004).

C. Johnson, H.-J. Sung, S. M. Lessner, M. E. Fini, and Z. S. Galis, “Matrix Metalloproteinase-9 Is Required for Adequate Angiogenic Revascularization of Ischemic Tissues. Potential Role in Capillary Branching,” Circ. Res., 94, 262-268 (2004).

J. J. Khatri, C. Johnson, R. Magid, S. M. Lessner, K. M. Laude, S. I. Dikalov, D. G. Harrison, H.-J. Sung, Y. Rong, and Z. S. Galis, “Vascular Oxidant Stress Enhances Progression and Angiogenesis of Experimental Atheroma,” Circulation, 109, 520-525 (2004).

S. M. Lessner, H. L. Prado, E. K. Waller, and Z. S. Galis, “Atherosclerotic Lesions Grow Through Recruitment and Proliferation of Circulating Monocytes in a Murine Model,” Am. J. Pathol., 160, 2145-2155 (2002).

E. Ivan, J. Khatri, C. Johnson, R. Magid, D. Godin, S. Nandi, S. M. Lessner, and Z. S. Galis, “Expansive Arterial Remodeling Is Associated with Increased Neointimal Macrophage Foam Cell Content. The Murine Model of Macrophage-rich Carotid Artery Lesions,” Circulation, 105, 2686-2691 (2002).

S. M. Kaska, S. Sarangapani, and J. Giner, "Oxygen Reduction on Platinum in Borate-Buffered Saline Solutions," J. Electrochem. Soc., 136 (1), 75-83 (1989).

Z. S. Galis and S. M. Lessner, “Inflammation and Matrix Metalloproteinases in Atherosclerosis,” In Vulnerable Atherosclerotic Plaque, Virmani, R., Narula, J., Naghavi, M., Casscells, S. W., and Willerson, J. T., eds., Atlas of Non-tumor Pathology, American Registry of Pathology (in press).