Faculty Member

Scientific Interests

Bradford Berk, MD, PhD

Working to understand the relationship between key blood proteins and atherosclerosis. The aim is to prevent white blood cells from entering blood vessel walls, where they "eat" cholesterol and cause inflammation. Most experts now believe that heart attacks are caused when the immune system attacks cholesterol as a foreign invader, causing inflammation with the potential for a diseased blood vessel to swell shut.

Mark Taubman, MD

Focused on the role of muscle cells that line blood vessel walls in controlling inflammation and the tendency for blood clots to form. Also looking into the role of circulating proteins (e.g. chemokines and tissue factor) in the body's response to injury, and how the healing process itself may contribute to heart disease.

Burns Blaxall, PhD

Looking at whether fear and rage can be harnessed to combat congestive heart failure. The team is focused on the genes that code for the chemical reactions involved in the body's "fight-or-flight" response. The human heart beats faster and stronger as adrenaline combines with beta adrenergic receptors (bARs) on heart muscle cells.Can bARs be used to make weak hearts beat faster?

Jun-ichi Abe, PhD

During a heart attack, lack of oxygen in the blood (hypoxia) and molecules that tear up cellular building blocks (oxidative stress) cause damage. Looking at the role played by mitogen-activated protein (MAP) kinases, a family of enzymes that switch on and off basic cellular functions like inflammation and the process by which diseased cells "decide" to self-destruct (apoptosis).

Jeffrey Alexis, MD

Focused on biochemical signals involved in transplant arteriopathy, where the immune system attacks the arteries of a newly transplanted heart. Arteriopathy, marked by inflammation around lesions like those seen with atherosclerosis, is the leading cause of death among transplant patients. Peroxisome proliferator-activated receptors (PPARs), which create peroxisomes to rid cells of toxic substances, may be useful in preventing arteriopathy.

Keigi Fujiwara, PhD

Key question: how do cells lining blood vessels sense and react to physical forces (as opposed to biochemical signals). The speed and force of blood flow dragging over cells, for instance, sets off complex cascades of reactions that play a role in heart disease. Mechanical forces indirectly impact cellular adhesion molecules (CAMs), for example. Researchers hope to manipulate CAMs to prevent white blood cells from entering and sticking to blood vessel walls, an early step in coronary artery disease.

Coeli Lopes, PhD

Interested in how the heart's electrical system maintains the force needed to pump, reset, and pump again in the normal rhythm. The timing of heart's electrical signal to pump depends on the movement of charged particles, or ions, through channels in heart cell membranes, which decide what moves in and out of a cell. The goal is understand the chemical signals that retard charged particle movement through ion channels to prevent sudden cardiac death.

Arthur J. Moss, MD

Investigating the exact causes of cardiac arrhythmias that cause many sudden deaths in children. Hundreds of related genetic mutations have been identified and landmark research continues on the dramatic lifesaving ability of implantable cardioverter defibrillators (ICDs). Now that the genes involved are documented, researchers are exploring how small changes in those genes can either increase or decrease risk of death.

Joseph Miano, PhD

Genes direct the construction and function of muscle cells lining blood vessels. In atherosclerosis, changing gene profiles can cause smooth muscle cell development to spiral out of control in a way reminiscent of tumor growth. The Miano lab is exploring the changes seen in the expression of genes in the presence of disease. Much of the work involves promoterology, the study of DNA promoter sequences that start the process of turning the information coded in genes into functional proteins.

Jane Sottile, PhD

The extracellular matrix is support tissue that, like bone, was once thought to be no more than inactive scaffolding that supports tissue shape. New evidence suggests the matrix is a complex mix of molecules that direct cell activity. The matrix may play a role in vascular remodeling, the lifelong process by which blood vessels change shape to keep blood flowing as they cope with atherosclerotic injury. In particular, Dr. Sottile's team is exploring the role of matrix protein fibronectin in vascular remodeling and related disease.

R. James White, PhD

Working to understand causes of vascular remodeling in severe pulmonary hypertension. Vascular remodeling changes blood vessel shape, making it harder to push blood through the vessels and increasing blood pressure. When this happens to blood vessels supplying the lungs, it is pulmonary hypertension. Basic experiments are helping Dr. White's team to understand how altered cellular growth and migration play a role in the vascular pathology of pulmonary hypertension.