The 2021 celebration of USF Health research was a fully virtual event
The arteries, veins and capillaries making up our vasculature supply blood and other essential substances to all organs of the body. And abnormalities affecting vascular biology are common across many disciplines and research areas emphasized at USF Health, including cardiac and pulmonary diseases, diabetes, metabolic disorders, maternal-fetal medicine, neuroscience and central nervous system diseases, and pharmacology.
So, this year’s Roy H. Behnke, MD, Distinguished Lecturer – an expert in blood vessel function and vascular disease – was particularly relevant to the audience of faculty, staff and students joining his online keynote presentation via Microsoft Teams. William C. Sessa, PhD, the Alfred Gilman Professor of Pharmacology and Medicine (Cardiology) and Director of the Vascular Biology & Therapeutics Program at Yale School of Medicine, spoke about “The vascular endothelium: interfacing lipids with cardiovascular risk.”
Stephen Liggett, MD, associate vice president for research at USF Health and vice dean for research at the Morsani College of Medicine, welcomed the audience before introducing Dr. Sessa. “This year will be a little different,” Dr. Liggett said. Due to COVID-19, all judging of poster presentations occurred online in advance of the Feb. 26 all-virtual event, and there were no oral presentations.
Despite this, as in years past, USF Health Research Day 2021 remained a celebration of the best scholarly work of students, residents, and faculty across USF Health, as well as health sciences collaborations with other USF colleges.
Dr. Sessa’s research has defined the molecular aspects and physiological implications of endothelial nitric oxide synthase (eNOS) activation and how eNOS regulates angiogenesis (blood vessel growth), vascular permeability, atherosclerosis, and vascular remodeling.
Speaking from his Yale office, Dr. Sessa framed his keynote address by saying that strides have been made in reducing cardiovascular risk with medications to control blood pressure, cholesterol-lowering statin drugs, and modification of lifestyle factors such as diet and exercise. Despite this progress, cardiovascular disease remains the number 1 cause of death in the Western world. An American Heart Association analysis projected that the total direct costs (medical expenses) and indirect costs (lost productivity) of cardiovascular disease in the U.S. alone would grow from $555 billion in 2016 to $1.1 trillion in 2035. So innovative, more precise treatments are urgently needed to reduce the incidence of atherosclerosis and other cardiovascular diseases.
Dr. Sessa provided an overview of his laboratory’s studies looking at the role of lipids (which include cholesterol and triglycerides) in vascular function, identifying new therapeutic targets that may impact lipid-endothelial cell interaction, and how triglycerides and fatty acids influence the balance between blood vessel injury and repair (vascular homeostasis).
The development of atherosclerosis, a vascular disease that can lead to excessive blood clotting and heart attack, is triggered by lipids in the plasma, or fluid portion of blood. Many thought leaders in the field agree that the transport (uptake) of low-density lipoprotein, or LDL (sometimes called “bad” cholesterol), across the endothelium (cells lining the inside of arteries) as well as its retention and accumulation in subendothelial spaces helps kindle the “inflammatory response bonfire” in vessel walls, ultimately causing the growth of atherosclerotic lesions, or plaques. Dr. Sessa said.
Most cholesterol medications work largely by lowering LDL levels in the blood. Among other areas of inquiry, Dr. Sessa’s group at Yale is looking for new signaling pathways (LDL-receptor independent) that may regulate the blood vessel LDL uptake that drives atherosclerosis. The researchers discovered that genetic loss of ALK1, a receptor highly expressed in primary human endothelial cells, reduces atherosclerotic plaques. More recently, they screened several candidate monoclonal antibodies in human endothelial cells and preliminary mouse model work indicates that, by neutralizing ALK1-mediated LDL uptake, the antibody treatment may significantly reduce initiation of atherosclerosis.
In his closing remarks directed to trainees, Dr. Sessa shared some medical research lessons he has learned throughout his career (see below). Among them: “This is an unprecedented time for research. Technological limitations are diminishing, so use your imagination and think big!”
The virtual celebration of research concluded with the announcement of the poster presentation winners. To see all the award winners, plus Research Day sponsors and donors, please Click Here.