They are developing new treatments to mitigate cardiovascular pathologies induced by obesity and diabetes and unique trans-tissue drug delivery systems for localized treatments to prevent diabetic foot ulcers. Their efforts are also directed at developing a lung treatment to mitigate chronic infection and inflammation in the lower airways of the lungs via localized deep-tissue drug delivery. Past research from the Pulakat Lab identified cardiac-specific cytokine and microRNA markers associated with the progression of diabetes and in response to treatment with Rapamycin, an anti-aging drug. They also elucidated the structure-function relationship of cardiovascular reparative Angiotensin II (Ang II) receptor AT2R and novel signaling networks of the AT2R that can mitigate the progression of heart disease and vascular damage caused by diabetes and obesity.

Current projects include:

The Kapur Lab was the first to establish that reduced endoglin activity improves survival and limits maladaptive cardiac remodeling in heart failure. The laboratory identified that targeting endoglin using an antibody-mediated approach limits and reverses established cardiac fibrosis in preclinical models of heart failure and acute myocardial infarction. The Kapur Lab was the first to identify that acute mechanical unloading of the left ventricle activates a cardioprotective signaling program in the setting of acute myocardial infarction and the first to identify novel molecular mechanisms regulating cardiac biology and mitochondrial function with extracorporeal membrane oxygenation (ECMO). Dr. Kapur is an inventor on multiple issued patents several of which have formed the basis for new companies.

Current projects include:

A major area of interest is the role of the hormone aldosterone and the receptor by which it functions, the mineralocorticoid receptor (MR), in the molecular mechanisms of cardiovascular disease. The steroid hormone aldosterone is the final step in the renin-angiotensin-aldosterone pathway that regulates blood pressure and electrolyte homeostasis by activating MR in the kidney to regulate genes involved in renal sodium handling. We and others have demonstrated that MR is expressed in cells of the human blood vessel, supporting the possibility that direct effects of aldosterone on the vasculature could play a role in vascular function and disease. This is clinically significant because, in human clinical trials, pharmacologic inhibition of the MR prevents heart attacks, strokes and cardiovascular deaths with minimal effects on systemic blood pressure.

A second major area fits in the field of cardio-oncology. The Jaffe lab is exploring the impact of cancer treatment on blood vessels and how this might contribute to side effects in cancer survivors. We are exploring the molecular mechanisms for these clinical findings in order to gain a better understanding of the mechanisms of cardiovascular disease and to identify novel therapeutic drug targets for common vascular diseases or to protect cancer patients from adverse side effects.

The Jaffe laboratory routinely uses in vitro molecular and cellular biology methods, primary human vascular cell culture models, state-of-the-art transgenic mouse models with in vivo capabilities to study rodent models of cardiovascular physiology and disease, unbiased transcriptomics, proteomics, and epi-genomics methods, and translational studies utilizing human samples from our patients across Tufts Medicine.

Current projects include:

Current projects include:

The Good Lab takes an interdisciplinary approach encompassing fundamental molecular and cellular biology, in vivo state-of-the-art imaging technologies, ex vivo vascular function techniques, and in vivo pathophysiological models to further our understanding of how blood flow regulation and inflammation contribute to the etiology of neurological diseases and to dissect the role of arterial and venous endothelial Panx1 in ischemic stroke and Alzheimer’s Disease.

Current projects include:

Using whole animal physiology, in vivo electrical stimulation of the heart and echocardiography, we study the predisposition of the heart to develop lethal arrhythmias and its association with diastolic dysfunction (heart failure with preserved ejection function, HFpEF). On the cellular level, we use isolated cardiomyocytes from these animal models, for cellular electrophysiology studies and direct measurements of calcium transients to measure abnormalities of repolarization, dysfunction and distribution of ion channels, and calcium dyshomeostasis in the predisposition to the development of ventricular arrhythmias. Using molecular biological tools, we study the role of second messenger signaling in the regulation of ion channel activity in the predisposition to ventricular arrhythmias, and development of diastolic dysfunction. We also have an interest in the role of Toll-Like receptors in the pathogenesis and treatment of mouse models for abdominal aortic aneurysms.

Current projects include:

Cardiovascular disease (CVD) remains the leading cause of death around the world and its incidence increases greatly with age in both males and females. However, the rate of CVD development increases significantly more in postmenopausal females. Our efforts are focused on identifying alternative strategies outside of hormone replacement therapy to mitigate CVD risk in aging women, and potentially men, as our approaches allow for the direct comparison of males and females and potential therapeutic targets that we identify may also aid in male CVD.

For these studies, we routinely utilize our state-of-the-art transgenic mouse models, in vitro molecular and cellular biology techniques, ex-vivo resistance vessel reactivity via wire myography, in vivo telemetric blood pressure measurements and in vivo cardiac and vascular imaging. Additionally, our laboratory also performs clinical studies examining vascular function in several populations. For these studies, we measure 1) microvascular function in the cutaneous circulation via laser Doppler flowmetry coupled with intradermal microdialysis and 2) arterial stiffness via applanation tonometry. Thus, we are a truly translational laboratory with studies spanning from the bench to the mouse to the human.

Current projects include:

Isabelle Reveillaud-Draper earned her PhD. in Biochemistry from the Université Montpellier 2/ Sciences et Techniques, Montpellier, France, studying the structural organization of small nuclear ribonucleoproteins. She then joined Dr. Tom Kornberg's laboratory at the University of California, San Francisco, for a post-doctoral position working on Drosophila development. As a research associate at the Linus Pauling Institute of Science and Medicine in Palo Alto, CA, she pioneered the expression of mammalian genes in transgenic Drosophila (i.e., mutant flies expressing the bovine superoxide dismutase) to facilitate investigations of the free radical theory of aging.