The Hope Heart Program at The Benaroya Research Institute

The Hope Heart Program was founded in 2004 when primary investigators, and their teams, from The Hope Heart Institute joined the labs at the Benaroya Research Institute at Virginia Mason. The marriage of the two research programs created The Hope Heart Program and launched a new chapter in basic scientific research. The program is part of The Hope's bench-to-bedside philosophy for combating heart disease.

The Department of Vascular Biology led Tom Wight, PhD. The department focuses on understanding the regulation of angiogenesis and vasculogenesis - two processes by which capillaries and larger blood vessels are formed.

The Department of Translational Medicine and Public Health led by Margaret Allen, MD.

The Hope Heart Program is focused on diseases of the cardiovascular system – the heart and blood vessels – and includes research at both the basic science and translational levels. To design therapeutic agents that can regulate blood vessel growth and regeneration of heart/vascular tissue requires a greater understanding of how these processes work in health and disease. Our various approaches include the analysis of atherosclerotic plaque, repair of tissue damaged during a heart attack, construction of artificial blood vessels, and characterization of macromolecules (proteins, proteoglycans) that participate in the extracellular regulation of cell behavior. Such "extracellular matrix" components are analyzed functionally in models of human disease that include obesity, atherosclerosis, wound healing, heart attack and cancer. Notably, researchers of the Hope Heart and Immunology Programs at BRI are working together to understand how disregulation of the immune system (autoimmune disease) contributes to cardiovascular disease. Such multidisciplinary collaborations between scientists are a hallmark of research at BRI.

In atherosclerosis, patients develop a thickened layer of cells and extracellular matrix (ECM) referred to as a neointima, which can obstruct blood flow. Neointima that are mechanically weak can break loose from the blood vessel wall (rupture) and block blood flow completely. Inducing the production of the ECM protein elastin in the neointima can inhibit its growth and strengthen it to protect against rupture, as shown above. A) Normal, uninjured model artery with elastin layers (arrows). B) After 4 weeks, an injured model artery develops a proliferative, greatly-thickened neointima (double-headed arrow) with no organized elastin layers. C) An injured model artery treated to inhibit the function of the ECM proteoglycan versican. Compared to the injured, untreated artery shown in panel B, the neointima of the injured, treated artery (double-headed arrow in panel C) is thinner and is strengthened with layers of elastin (arrows), like those in the uninjured artery shown in panel A.