Research Advancements

2019 Research Grants

Jocelyn Beard Moran Memorial Fellowship
AWRP 2018 AHA Institutional Research Enhancement Award (AIREA)

                                    Elena Galkin, PhD
Eastern Virginia Medical School
Norfolk, VA

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

Atherosclerosis is the leading cause of cardiovascular disease, the leading cause of death in the US.  B cells are a type of white blood cell in the body responsible for making antibodies, which are blood proteins produced in response to counteracting a specific foreign substance in the blood.  Though much is known about the general role of B cells in atherosclerosis, very little is known specifically how B cell receptor signaling affects B cell functions within atherosclerosis. Specifically, understanding how lipid uptake occurs in mobile white cells, also called macrophages, we can demonstrate how this process is critical in the development of atherosclerosis. Through better understanding the role of B cell function, our work will help to change existing models, with goals of uncovering new potential therapeutic targets of atherosclerosis.

 

Donna Gaff Marriott Award
Summer 2018 Predoctoral Fellowship

Federick Zasadny, BSE MS
George Washington University
Washington, DC

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

Our research seeks to better understand energy distribution and demand process across a heart.   By directly quantifying the changes when heart rate is increased, we can begin to better understand how the energy supply and demand processes in the heart are synchronized. The ultimate goal is to understand the process in damaged hearts in patients with heart failure.   During the last five years, imaging technologies used on satellites in space have been miniaturized and made affordable by advances in nanofabrication. Our research seeks to harness these advances to image hearts with failing tissue and understand how the heart distributes energy when it is required to work harder.  This will allow clinicians to better understand how the heart responds under high workloads, such as during exercise. This is an important development that will possibly replace current diagnostic assumptions that do not look at energy modulation as a major therapeutic area in heart failure.

Anne Davis Camalier Award
2018 Transformational Project Award

Giulio Agnetti, PhD
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 the cause for the organ failure could be the formation of toxic substances, known as misshapen proteins. Misshapen proteins can have a tendency to group and rearrange to form toxic structures, which can cause tissue damage.   Currently, the identity of the misshapen protein in the heart is not known. We generated evidence that the protein “desmin” is prone to become misshapen in the heart, and we will study the toxic effect of this change over time as well as potential novel therapy.  The discovery of a mechanism that is independent of genetic mutations would allow the creation of different targeted diagnostics and treatments that could help prevent and cure HF.

Maggie Wimsatt Memorial Award

Patrick Calhoun, BS
VT Carilion Research Institute
Virginia Polytech Institute

Heart disease has been the leading cause of death in the United States for over 100 years. An important aspect of all forms of heart disease is a loss of proper cell-to-cell communication. The mechanism by which a virus disrupts this communication may be the same mechanism by which normal healthy hearts become diseased. Specifically, we will study a virus that infects human hearts and is capable of altering cell-to-cell communication. By controlling the cell-to-cell communication in a laboratory setting, we can assess how the virus may impact this process, as well as better understand similar dynamics in the absence of a viral infection. Understanding this mechanism will allow for therapeutic intervention and hopefully will significantly relieve the burden of cardiovascular 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

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.

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ANNE DAVIS CAMALIER AWARD

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.



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WOMEN’S BOARD AWARD


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.

WOMEN’S BOARD AWARD


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.