Research Advancements

2019 Research Grants

AWRP 2018 AHA Institutional Research Enhancement Award (AIREA)

Eastern Virginia Medical School
Norfolk, VA

Modified LDL uptake, B cell receptor signaling, and atherosclerosis:

Atherosclerosis is the leading cause of the cardiovascular disease, the leading cause of death in the US. Though atherosclerosis is a multifactorial disease current therapies only target one of the many arms of the disease. And though much is known about the general role of B cells in atherosclerosis, very little is know about how B-cell receptor signaling affects B cell functions within atherosclerosis. Our study hopes to help forge new lines of investigation in determining for atherosclerosis develops and to hopefully provide potential therapeutic options.

For years, macrophages taking up modified lipids have been at the heart of the development of atherosclerosis. We show for the first time in our study that B cells can take up these modified lipids as well. Furthermore, we show that unlike macrophages that become activated upon lipid uptake, B cells seem to down regulate the inflammatory process. We plan to investigate this by looking at well characterized pathways and examining how the B cells ability to respond to these antigens is down regulated if they have taken up these modified lipids. This is important because it provides the field a potentially new therapeutic target for preventing and treating atherosclerosis. Additionally, we will be using genetically modified mice that will also be used to test the role of CD45 in atherosclerosis and how the strength of signaling can affect energy, tolerance, and activation thresholds. In short, we will use mice that are B-cell deficient and prone to atherosclerosis and inject these mice with B cells that are either normal or have low levels of CD45 expression. After 12 weeks on a western diet we will examine atherosclerosis development in these mice. This work will be fundamental to elucidating how the B cell is modulated in the induction of atherosclerosis.

Summer 2018 Predoctoral Fellowship

George Washington University
Washington, DC

Rapid spectral mapping of ventricular absorbance to quantify homeostatic energetics in failing hearts:

I propose to address the major problem of not being able to quantitatively understand energy distribution in hearts with failing tissues. Within the last 5 years, imaging technologies used on satellites in space have been miniaturized and made affordable by advances in nanofabrication. I am proposing to harness these advances to image hearts with failing tissue to understand how the heart distributes energy when it is required to work harder. Direct visualization of these processes has not yet been achieved. Indeed, the visualization will allow clinicians to better understand how the heart responds under high workloads, such as during exercise. Patients with abnormal heart tissue will receive better care by the clinicians who better understand the energy distribution system in the heart.

I want to be able to directly quantify the changes in energy distribution in the heart when heart rate is increased. In this way, we can begin to better understand how the energy supply and demand processes in the heart are synchronized, and how they are damaged in patients with heart failure. I will use a high speed imaging system that will capture light passing through the heart that represents energy distribution changes inside cells and thus across the heart. I propose the amount of light passing through the heart depends on the energetic demand in the heart. The images collected from the heart will be analyzed for alterations in energy distribution. Understanding how the alterations occur will also be analyzed by modulating specific energy demanding processes.

2018 Transformational Project Award

Johns Hopkins University of Medicine
Baltimore, MD

Novel Mechanisms and Therapies for Proteopathic Heart Failure:

Despite the fact that Heart Failure (HF) represents a major cause of morbidity and mortality in Westernized countries, the molecular reasons underlying the decrease in the function of the heart with the progression of the disease are still unclear to date. There is an emerging consensus that, not unlike Alzheimer’s, the cause for the organ failure could be the formation of toxic, misshapen proteins. However, unlike Alzheimer’s , Parkinson’s, etc. the identity of the misshapen proteins in the heart is not known to date. We generated evidence that the protein Desmin is prone to become misshapen in the heart and we will now study the toxic effect of this change over time as well as the toxicity of misshapen Desmin and a novel therapy.

Misshapen proteins can have a tendency to group and rearrange to form toxic structures called Preamyloid Oligomers (or PAOs). Through the toxicity of these PAOs in other diseases, such as Alzheimer’s and Parkinson’s, is relatively well-established, it is unclear how they could be toxic for the heart. Therefore, we will define the temporal association between Desmin PAOs formation and disease, and investigate a likely mechanism for their toxicity at the cellular level: the negative effects of PAOs on the function of mitochondria, the powerhouses of the cell. We will also test the therapeutic potential of a natural compound that has shown promise in our preliminary studies as well as in clinical studies on Alzheimer’s disease.

2017 Grant Recipients

Mamie Doud Eisenhower Memorial Award

Honoring the former First Lady’s 25 years of devoted service to the Women’s Board

Matthew Barberio

Children’s Research Institute
Washington, DC

AWRP Winter 2017 Postdoctoral Fellowship

Our research addresses a potential mechanism by which youth obesity results in early-onset atherosclerotic development, a major risk factor for CVD and stroke. The studies are designed to understand the role of adipocyte-derived exosomes (specialized vesicles that are derived from fat cells) as well as the role of exosomal microRNA on suppressing cholesterol efflux gene expression. While the atherosclerotic cardiovascular disease is the leading cause of adult mortality, sub-clinical atherosclerosis is detectable in obese youth. Thus, understanding these processes in youth may help identify at-risk individuals. Identifying a novel mechanism and a biomarker for early detection will result in the foundation for primary prevention and treatment of CVD risk and allow children to live longer, healthier lives.

Jocelyn Beard Moran Memorial Fellowship

Honoring the founder of the Women’s Board


Che-Ying Kuo
University of Maryland
College Park, MD

AWRP Winter 2017 Predoctoral Fellowship

The purpose of our research is to investigate the mechanisms regulating the pathology of preeclampsia (PE), the elevated blood pressure during pregnancy. PE is the leading cause of maternal and perinatal morbidity and mortality affecting 3 to 8% of all pregnancies and it has been linked to increased risk of developing heart disease later in life for the mothers. In addition, recent research suggests that babies develop coronary heart disease, hypertension, and type 2 diabetes, originate from intrauterine growth restriction in which is caused by preeclampsia. We would like to understand ask are how does epidermal growth factor (EGF) regulate the development of preeclampsia. Despite the efforts to better understand the pathogenesis of preeclampsia, no effective treatment is available today other than early delivery of the fetus and placenta prematurely. In addition, there’s a lack of effective clinically relevant early predictor for preeclampsia, which will improve disease management.

Donna Garff Marriott Award

Honoring many years of service to the Women’s Board

Linhao Ruan

Ruan Linhao
Johns Hopkins University School of Medicine
Baltimore, MD

AWRP WINTER 2017 Predoctoral Fellowship

Heart failure is common, costly, fatal and disabling. Current treatment options improve symptoms and prolong life, but do not address the fundamental problem of the loss of functional heart muscle. Although studies have been done to assess whether injecting regenerative (stem) cells into the heart improves heart function, none have been shown conclusively to be effective. Our research involved a way to print heart muscle using a special 3D printer, that uses heart cells (made from patient’s stem cells) and other supporting cells. We have studied 3D printed heart patches and their structural and functional properties. This proposal seeks to optimize the structural and functional properties of these tissues, in an effort to create cardiac disease models and reagents for myocardial repair. This is essential to the ultimate development of the use of stem cells in cardiac repair and identifying new therapeutic targets.



Honoring steadfast commitment to the Women’s Board 

Michael Schar

Johns Hopkins University School of Medicine
Baltimore, MD

AWRP WINTER 2017 Scientist Development Grant

Endothelial dysfunction occurs when blood vessels are not able to increase the size to meet demands for stress with increased blood flow. This dysfunction predicts future bad events such as cardiac infarction or stroke. To measure endothelial function, a “barometer” of vascular health, in arteries of the heart patients traditionally had to undergo an invasive catheterization procedure where a tube is put into the vessel to deliver X-ray visible dye into the heart. Our research introduces a noninvasive technique to measure the vessel size using magnetic resonance imaging (MRI). The goal of our research is to make the noninvasive MRI technique to measure vessel size more robust and tolerable for more patients and will then allow testing, without invasive catheterization, whether the vessels are healthy and whether their health improves after taking new medications or after lifestyle changes.



Katherine Owsiany

University of Virginia
Charlottesville, VA

AWRP WINTER 2017 Clinical Health Profession Student Training Program

It is thought that the response of immune cells and muscle cells might be the key factor that determines if the arterial damage is repaired or left vulnerable. Inflammation has been recognized as a key factor that drives arterial damage. Muscle cells were thought to help heal the damage, but our lab has recently discovered that the muscle cells can be inflammatory and might cause damage as well. Our research will focus on whether muscle cells can make a protein that is a signal to activate the negative effects of immune and muscle cells, called MCP1. The clinical trials and dose of a drug that blocks MCP1 were designed to target immune cells, but efforts were abandoned almost ten years ago after modest results. The key question in light of the current knowledge in the field is to determine if muscle cells are able to act like immune cells enough to cause arterial damage, but not enough to be susceptible to the same drugs. The answer could provide extraordinary impact, not only by providing a route for innovative therapies but making existing therapy more effective.


Xi Lan

Johns Hopkins University School of Medicine
Baltimore, MD

AWRP 2017 WINTER Postdoctoral Fellowship

Intracerebral hemorrhage (ICH) is a type of stroke that occurs when a blood vessel bursts in the brain and can cause death or lifelong disability. A protein called soluble epoxide hydrolase (sEH) plays an important role in ICH. Our research evaluates the role of sEH and will determine whether sEH can become a new therapeutic target in the treatment of this type of stroke. The substance, TPPU, is a sEH inhibitor, which might become a promising candidate drug to treat ICH. We will investigate the effects and mechanisms of sEH inhibition in ICH, and develop new therapies of ICH. Our long-term goal is to find a drug or therapy that can be used to treat intracerebral hemorrhage-induced brain damage and help patients to heal faster and more completely. Investigating the role of sEH in ICH will help us to find a new therapeutic way.