Michael Autieri, PhD
The long-term focus of our research program is the identification and characterization of proteins and pathways which play a role in regulation of vascular inflammation, with a current focus on the role of endogenous anti-inflammatory cytokines in this process. We have two distinct but related areas of investigation: inhibition of vascular occlusive diseases such as atherosclerosis, restenosis and allograft vasculopathy; and promotion of angiogenesis to treat peripheral vascular disease. Currently, we are focusing on an endogenous anti-inflammatory cytokine termed IL-19 which: regulates macrophage polarity, macrophage and smooth muscle cell cholesterol homeostasis, smooth muscle and endothelial cell proliferation, and decreases inflammatory mRNA stability, suggesting that this cytokine may represent a therapeutic modality to treat vascular inflammatory diseases.
Wen (Xiongwen) Chen, PhD
- Ca2+ regulation of gene expression, mitochondria and energy production, protein synthesis and degradation, molecular trafficking and localization, myocyte proliferation and maturation in normal and diseased hearts.
- The role of smooth muscle cell Ca2+ signaling in hypertension and atherosclerosis. We are using a transgenic mouse model with increased Ca2+ influx into smooth muscle cells for this study.
- The roles of EPAC and PKI/PKA in heart disease development: we are trying to unveil novel aspects of cAMP signaling by studying the balances between EPAC and PKA, and between PKI and PKA, in cardiac physiology and pathology. Based on the mechanistic study, we will perform translational studies using AAV vectors to overexpress PKI in stressed hearts to ameliorate heart disease development.
Daniel Dries, MD
We are examining the genetic and non-genetic factors that influence the cardiac natriuretic peptides system regulating the cardiac response to stress including hypertension. We have a particular focus on the importance of natriuretic peptide processing. We are also studying the role of the Unfolded Protein Response, in particular RIDD, in Stage B and C heart failure and its interaction with the endogenous natriuretic peptide system and other relevant molecular pathways.
Satoru Eguchi, MD, PhD
The Eguchi lab studies mechanisms of cardiovascular disease using several distinct model systems. We infuse mice with angiotensin II to induce hypertension associated with organ damage including cardiac hypertrophy, vascular hypertrophy, cardiac fibrosis and vascular fibrosis, and abdominal aortic aneurysm in mice. In addition, we study the signal transduction mechanism of vascular smooth muscle and endothelial cell pathophysiology. Our current research subjects include angiotensin II receptor, EGF receptor signal transduction, ER stress, mitochondrial dynamics and autophagy.
Steven Houser, PhD
The research in the Houser laboratory is focused on those processes that maintain the electrical and contractile properties of the normal heart and the defects in these processes that lead to electrical instability (arrhythmias and sudden death) and poor cardiac pump performance (congestive heart failure). We are currently continuing our studies of the determinants of cellular electrical and mechanical defects in diseased cardiac myocytes. In addition, we are exploring the idea that a major factor that determines the overall state of cardiac myocyte function is a balance between new myocyte formation (cardiac regeneration) and programmed myocyte death (apoptosis). We are exploring the idea that activation of Ca2+ dependent signaling pathways (mainly through CAMKII) regulates Ca2+ handling proteins in diseased myocytes. We have recently identified a novel stem cell that resides within cortical bone.
Joon Park, PhD
My research has been focused on determining the molecular basis of exercise effects in vascular disease and function. Current research projects focus on answering such questions as: How can the physiological changes during exercise be defined at the cellular level? How do cells respond to the stimulus? What mediates cellular responses to the stimulus? And, how do cells adapt to the stimulus when it persists repeatedly and chronically? Specifically, 1. Role of p53 in mitochondrial remodeling in response to fluid shear stress in vascular endothelium; 2. The signaling mechanism of angiotensin II-induced hypertensive vascular remodeling; 3. Identifying a novel cellular biomarker produced by cerebrovascular endothelium in response to mild head impact in human; 4. Role of mitochondrial dynamic events on myogenic differentiation
Fabio Recchia, PhD
My laboratory is studying, in large animal models, the role of factors released by heart and skeletal muscle and named, respectively, “cardiokines” and “myokines”, as modulators of cardiac function and metabolism under physiological and pathological conditions. A second line of experimental research is on new pharmacological and biological therapies for the treatment of heart failure and atrial fibrillation.
Victor Rizzo, PhD
The long-range goal of the Rizzo lab is to discover the molecular signaling mechanisms that contribute to endothelial dysfunction and associated cardiovascular diseases such as atherosclerosis and aneurysm formation. Past studies demonstrate the importance of caveolae organelles in regulating endothelial cell function. Our research program offers the opportunity to evaluate the physiologic and pathophysiologic roles of endothelial caveolae and caveolin in signaling and transport using modern techniques in microscopy, biochemistry, cell biology, molecular genetic and unique in vivo and in vitro methodological approaches to attenuate vascular disease initiation and/or progression.
Abdelkarim Sabri, PhD
Our lab studies the molecular and cellular basis of heart failure, with a particular emphasis on the role of inflammatory mediators and innate immunity in disease progression in the failing heart. Our team examines how inflammatory mediators and innate immunity leads to pathological cardiomyocyte growth or programmed cell death and contributes to diseases such as cardiac hypertrophy, cardiomyopathy, and heart failure. Our long term goals are to provide novel insights about the molecular pathways that govern cardiac myocyte growth and function and to use this information to devise pharmacologic and genetic therapies for heart diseases in humans. Specifically: inflammatory serine proteases and cardiac repair, protease activated receptors in heart disease and 3-G protein coupled receptors and receptor tyrosine kinase crosstalk in adaptive and maladaptive cardiac hypertrophy.
Rosario Scalia, MD, PhD
- Project 1: We study the role of the microcirculation in the adipose tissue inflammation of the overweight/obese organism to: a) understand how nutrients and excessive calorie intake activates inflammatory signaling cascades in adipose tissue, and b) to find therapeutic targets to averts the metabolic and cardiovascular complications of obesity.
- Project 2: Regulation of endothelial function by Calpain. Specifically, we study the impact of calpaan activation on eNOS and endothelial cell adhesion molecule expression levels and functions. We have established the calpain system as an important modulator of endothelial function in insulin resistance and hyperglycemia.
- Project 3: We are interested in exploring the main signaling pathways through which physiological aging impairs key function of the vascular endothelium. The overall goal of this research is to find therapeutic targets to offset or delay cardiovascular disease and organ dysfunction in the aging organism.
Xiao-Feng Yang, MD, PhD
- Vascular immunology and atherosclerosis: Dr. Yang’s laboratory uses microarray transcriptome, next generation DNA sequencing including RNA-Seq, T cell epitope mapping, SEREX and other biochemical, immunological approaches and transgene/gene knock-out disease models in order to determine cardiovascular disease (CVD) risk factors, such as hyperlipidemia-, hyperglycemia-, uremia-, endotoxemia, impact the development/progression of vascular inflammation and atherosclerosis.
- Immunometabolism: Dr. Yang’s laboratory also aims to study how biochemical metabolites in CVD-related pathologies act as either danger signals or homeostatic signals to regulate antigen processing/presentation, vascular immune responses and atherosclerosis.
- Epigenetic pathology: Dr. Yang’s laboratory also studiese how CVD risk factors regulate histone modification process and gene expressions in vascular inflammation and atherosclerosis.